We read the letter from Dr Smith with interest and thank him for
suggesting his paper for discussion. Dr Smith argued that (i) there was
significant overlap between his study [1] and ours [2], and (ii) oxygen
desaturation as measured by pulse oximetry was an inappropriate means for
testing exercise desaturation. We strongly disagreed with both points.
We read the letter from Dr Smith with interest and thank him for
suggesting his paper for discussion. Dr Smith argued that (i) there was
significant overlap between his study [1] and ours [2], and (ii) oxygen
desaturation as measured by pulse oximetry was an inappropriate means for
testing exercise desaturation. We strongly disagreed with both points.
(i) Our study and that of Smith and Agostoni differed in aims,
patient selection, methods and, as a result, provided different
information relevant to current clinical practice. Our study compared a
validated quantitative measure of severity of chest x-ray changes (ILO
readings) with a readily available, quantitative measure of gas exchange
during exercise (arterial oxygen desaturation). We studied 38 subjects
with asbestosis diagnosed on the basis of exposure history, clinical signs
of asbestosis and typical HRCT appearances of asbestos-induced
interstitial fibrosis, in keeping with modern clinical practice [2].
The study of Smith and Agostoni did not do this. They separated 95
asbestos-exposed workers into those with asbestosis and those without.
The asbestosis group (n=27) included a mixture of patients with ILO
profusion > 1/0 as well as subjects with unexplained reduction in lung
volume or DLco, who did not have radiological evidence of asbestosis –
debatable inclusion criteria rarely used elsewhere. They then used
various measures of arterial oxygenation during rest and exercise to
discriminate those 27 patients from asbestos-exposed workers who did not
have asbestosis. The best of their measures, deoxygenation on exercise,
demonstrated modest discriminatory power. They then related this variable
to ILO profusion score for their complete patient group, making no
distinction between those with and without asbestosis [1].
Our study directly related resting lung function and a more
comprehensive ILO radiographic assessment (profusion, zones affected and
pleural thickening) to deoxygenation during exercise in independently
diagnosed asbestosis subjects and demonstrated a significant relationship
[2]. By multivariate analysis, we found that arterial oxygen desaturation
was independently predicted by a combined use of DLco, FEV1/FVC ratio and
the number of affected zones on ILO scoring. While the profusion score
correlated with oxygen desaturation on linear regression, it did not
remain significant in the multivariate analysis. Smith and Agostoni only
examined one ILO parameter, the profusion score, and multivariate analysis
was not conducted. Hence, we emphatically disagree with Dr Smith’s
suggestion that our paper ‘presents no new information’.
An important message from our study is that the extent of parenchymal
damage (number of zones affected) is correlated with resting pulmonary
function and is an independent predictor of exercise desaturation.
Previous studies of ILO scores have mainly focused on the profusion and
few, if any, have placed importance on the influence of the extent of
asbestosis on physiological impairment. Our findings are consistent with
recent studies showing that the area affected by pulmonary fibrosis as
quantified on HRCT correlates well with pulmonary function [3,4].
(ii) Dr Smith went on to argue against the validity of pulse oximetry
as a measure of gas exchange during exercise. Pulse oximetry is a
standard methodology, in commonplace use throughout the world because of
its validity and simplicity, displacing indwelling arterial lines, which
are invasive and have largely fallen into disuse for clinical purposes.
There seems little point to us, in attempting to provide guidance to
clinicians, to use methods that are unlikely to be readily available to
them.
Yours sincerely,
Y C Gary Lee MBChB PhD FCCP FRACP
Bhajan Singh MBBS PhD FRACP
S C Pang MBBS FRCP FCCP
Nicholas H de Klerk MSc PhD
David R Hillman MD FANZCA
A William Musk MD MS FCCP FRACP FAFOM FFOM
Correspondence:
Dr. Y C Gary Lee,
Wellcome Trust Centre for Human Genetics, University of Oxford, Roosevelt
Drive, Oxford OX3 7BN, U.K.
Tel: 01865-287579 Fax: 01865-287578
References
(1) Smith DD, Agostoni PG. The discriminatory value of the P(A-a)O2 during
exercise in the detection of asbestosis in asbestos exposed workers. Chest
1989; 95:52-5.
(2) Lee YCG, Singh B, Pang SC, De Klerk NH, Hillman DR, Musk AW.
Radiographic (ILO) readings predict arterial oxygen desaturation during
exercise in subjects with asbestosis. Occup Environ Med 2003; 60:201-206.
(3) Wells AU, King AD, Rubens MB, Carmer D, du Bois RM, Hansell DM. Lone
cryptogenic fibrosing alveolitis: A functional-morphologic correlation
based on extent of disease on thin-section computed tomography. Am J
Respir Crit Care Med 1997; 155:1367-1375.
(4) Wells AU, Hansell DM, Rubens MB, Cailes JB, Black CM, du Bois RM.
Functional impairment in lone cryptogenic fibrosing alveolitis and
fibrosing alveolitits associated with systemic sclerosis. Am J Respir Crit
Care Med 1997; 155:1657-1664.
The publication of "Radiographic (ILO) readings predict arterial
oxygen desaturation during exercise in subjects with asbestosis" by YCG
Lee et al. from the Sir Charles Gardiner Hospital in Perth [1] presents no new
information and fails to reference an earlier paper on the same subject
which included more patients with clinical asbestosis and four different
control groups.[2] This paper actually m...
The publication of "Radiographic (ILO) readings predict arterial
oxygen desaturation during exercise in subjects with asbestosis" by YCG
Lee et al. from the Sir Charles Gardiner Hospital in Perth [1] presents no new
information and fails to reference an earlier paper on the same subject
which included more patients with clinical asbestosis and four different
control groups.[2] This paper actually measured the P(A-a)O2 rather than
estimating it from the oxygen saturation. Furthermore it correlated the
change in A-a OO2 gradient with the amount of work performed during
exercise by measuring the P(A-a)O2/VO2 ratio which was more specific and
sensitive than the P(A-a)O2 gradient. The estimate of the true oxygen
tension by measuring pulse oximetry is fraught with potential error well
understood by most pulmonary physiologists including motion artifact,
vasoconstriction, hypotension, carboxyhemoglobinemia, methemoglobinemia
and anemia.[3] The same information contained in the paper by Lee et al is
available in a more comprehensive fashion in the earlier publication by
Smith and Agostoni.
References
(1) Lee YCG, Singh B, Pang SC, de Klerk NH, Hillman DR, Musk AW.
Radiographic (ILO) readings predict arterial oxygen desaturation during
exercise in subjects with asbestosis" Occup Environ Med 2003;60:201-206.
(2) Smith DD, Agostoni PG, The discriminatory value of the P(A-a)O2
during exercise in the detection of asbestosis in asbestos exposed
workers. Chest 1989;95:52-55.
(3) Sinex JE. Pulse oximetry: principles and limitations. Am J Emerg Med
1999;17:59-67.
The letter [1] by Professor Cherrie in this issue addresses the long-standing question as to whether static (area, stationary) samples can be
used to estimate exposure to people in lieu of personal measurements for
epidemiological investigations. In my previous letter [2] the question was
ask “are personal and static samples related?” and Cherrie [1] answered this
question as “yes”. As mentioned in my...
The letter [1] by Professor Cherrie in this issue addresses the long-standing question as to whether static (area, stationary) samples can be
used to estimate exposure to people in lieu of personal measurements for
epidemiological investigations. In my previous letter [2] the question was
ask “are personal and static samples related?” and Cherrie [1] answered this
question as “yes”. As mentioned in my previous letter [2] and recently by
Cherrie [3] there have been numerous studies [4-10] that evaluated the
“relationship” between static and personal air measurements. The vast
majority of studies [7] have suggested that there is no similarity in
comparison of personal and static samples, although a few [8] have reported
an association. However, these investigations directly compared
concentration reported [7] by the two measurement methods and do not consider
the effects of dilution in determining a ratio of concentrations. A
study [3] by Cherrie of personal and static samples in which he evaluated
investigations published in the Annuals of Occupational Hygiene during a
ten-year period found a personal to static concentration ratio of 1.5.
Another investigator [11] reported that when ventilation condition was
applied as good, fair and poor, ratios became 3.2, 3.0 and 1.5,
respectively. Cherrie’s study [3] along with others [4,8] that reported no
statistical difference in concentration between the two-measurement
methods support the concept of some relationship.
It must be noted that most reports comparing personal and static
samples are in relationship to occupational exposures.[5] Occupational
comparisons will be different from environmental exposures in that
occupational measurements are usually collected at the source of
contaminates (near field) and are commonly contained within a structured
environment. However, there are exceptions in that occupational
activities do occur in the general environment, such as on streets (e.g.
parking enforcement officers).
It is generally agreed [1,7] that personal samples exhibit a higher
concentration than static samples in the occupational environment. One
explanation for a lack of concentration relationship between personal and
static samples is the proximity to the emission source.[1,5] In general,
workers are near the emission source with their movement around the work
location. Static samples do not move from their placed location so they
will not exhibit differences in “exposure” concentrations as would be
associated with movement of a worker. Location of a static sampler in
comparison to movement and activity of a worker has been suggested to
greatly influence any relationship.[5] Other factors such as work
practices, episodic releases, air streams, and ventilation will also have
a major impact on the concentration collected by static samples and their
subsequent comparison with personal sample concentrations.[1,5] If static
samples are placed closer to the emission source they will exhibit a
higher concentration than personal samples, which does not represent
actual exposure to the worker.[12] Thus, placing of the static sample is
possibly of greater importance than ventilation and size of the room.
However, most static samples are placed outside the workers’ workstation
so as not to interfere with their activities and will exhibit a lower
concentration as a result of dilution caused by distance and ventilation
as well as effect from room size and configuration.
A major factor to consider in comparison of these sampling methods
that has not been well discussed is sample variability (geometric standard
deviation - GSD). When examining variability (table) in comparison
studies, static samples generally have a greater variability than personal
samples, although this is not universally consistant.[10] Why static
samples generally exhibit the larger variability is not clear; however,
may be related to stratified zone samples having a smaller variability.[12]
Greater variability provides less predictability of samples for future
exposure. However, the large variability observed for occupational
samples makes the increased variability in static samples somewhat moot in
that there is a large day-to-day variation.[13]
Table Comparison of variability in studies reporting a relationship
and no relationship for personal and static samples.
Study
Sampling
GM
GSD
Relationship
Lange
et al. 1996
Personal
0.089a (0.133b)
2.75
Not statistically different
8, x Static
0.097a (0.108b)
3.17
Lange
et al. 2000
Personal
0.005a (0.004b)
2.47a (2.00b)
Not statistically
different
5,x Static
0.002a (0.002b)
2.42a (2.03b)
Lange and
Thomulka, 2002
Personal
0.007
1.8
Not statistically different
4,x Static
0.013
2.4
Lange, 1999
Personal
0.021a (0.019b)
1.73a (1.66b)
Statistically different
7,x Static
0.005c
1.67c
Lange and
Thomulka, 2000
Personal
0.018a (0.015b)
2.81a (2.54b)
Statistically
different
16,x Static
0.007a (0.006b)
3.14a (2.73b)
Seixis
et al.
1997
Personal
0.20
2.23
Statistically different
10,y Static
0.13
2.38
Key
x – asbestos samples, in f/cc
y – mg/m3 of respirable dust
a – with outliers
b - without outliers
c – no outliers
When comparing environmental and occupational exposure sampling these
two differ in that environmental exposures are those which exhibit
contaminates to the entire community or within a home type setting while
occupational is strictly associated with employment activities in an
occupation. However, for some conditions there will be a considerable
overlap such as associated with persons working outdoors or locations that
are frequented by the public (e.g. shopping malls).
Environmental exposure sampling from near sources will likely result
in a similar relationship as seen with occupational sampling. Exposure
from far sources will on the other hand likely be similar since the
pollutant concentration will be more evenly dispersed due to mixing and
distance. However, this assumes that there is no trapping or
magnification of the contaminate in a building or location. These
explanations provide some suggestions as to the variations observed
between personal and static sampling and by including microenvironment
monitoring and modeling from diary information as suggested by Harrison et
al,[14] will allow establishment of a relationship. Some have pointed out
that use of static samples to predict exposure for epidemiological
evaluation is so flawed that environmental samples even after modeling are
not suitable for predicting personal exposures.[15] These two
publications [14,15] demonstrate the uncertainly associated with relating
personal and static samples by occupational hygienists and subsequent use
in epidemiological studies.
Since the source of contaminate is the same in occupational studies
and static samples are collected from the same population of pollutants
except experiencing a dilutant effect from the source there must be some
relationship.[8] This relationship is likely related to the individual
situations because of location of the source, work environment, worker
activity, and static sampling conditions. Since epidemiological studies
are interested in population effects and generally cumulative exposure, at
least for chronic toxicants, a general relationship between sampling
measurements is viable.[8] To better apply any relationship between these
sample methods, inclusion of a ventilation condition [11] or other summary
predictor of the sampling location would appear to be appropriate.
Cherrie [3] set forth a simple model for evaluating the relationship
between personal and static samples for uniformly mixed contaminates,
while Pundham et al,[11] incorporated ordinal conditions for establishing a
ratio. Cherrie’s ratio for personal to static samples in occupational
settings does not allow adjustment for variable conditions; thus, not
permitting adaptation of his model to complex occupational epidemiology
studies. The model proposed by Cherrie [1] should be modified for various
occupational settings where different conditions of the workplace
environment can be imputed. Thus, there needs to be a combination of the
model proposed by Cherrie [1] and conditions of the work environment as
suggested by Purdham et al.[11] However, development and future
implementation of Cherrie’s model [1,3] signify a new era in the old concept
of employing static samples for estimating exposure to affected
populations.
For environmental epidemiology scenarios I agree that a relationship
will exist as indicated by Harrison et al,[11] especially when evaluating
far field contaminates. This is especially true for contaminates that
have been well mixed in the environment. However, environmental static
samples will suffer from the same problems as occupational sampling in
that there will be cases of near sources (e.g. emissions from cooking
devices in homes – a point source)[17] Relationship of personal and static
samples in an environmental setting from a point source would be the same
as that seen in occupational studies. Thus, Cherrie’s [1] model would be
useful for these scenario’s as well.
As suggested by Cherrie [1] employment of personal samples has provided
great insight to exposure, disease and evaluating controls in occupational
health. His simple model is an excellent start to better understand the
relationship between the two forms of sampling. As mentioned by Cherrie [1]
there needs to be included a multitude of factors in predicting the
relationship of these forms of sampling. Most have considered that there
is no relationship and consider the subject matter not worth pursuing.
For this I disagree. A better understanding of a relationship between
personal and static sample concentrations will add insight to
environmental and occupational epidemiology and will allow use of
additional data in many epidemiological studies. As mentioned by
Professor Sarin,[17] statistical modelling will be required, as started by
Cherrie,[1,3] in establishing acceptable factor(s) of applying static
samples as a representative measure of exposure to a study population.
Clearly, additional research is needed to better understand the use of
static samples in determining exposure. Hopefully, this letter and the
one by Cherrie [1] will ignite such investigation.
(2) Lange JH. Are personal and static samples related? (Letter). Occup
Environ Med 2003 60:224-225.
(3) Cherrie JW. The beginning of the science underpinning occupational hygiene. Ann Occup Hyg 2003;47:179-183.
(4) Lange JH, Thomulka KW. Airborne exposure concentration during
asbestos abatement of ceiling and wall plaster. Bull Environ Cont Tox
2002;69:712-718.
(5) Lange JH, Kuhn BD, Thomulka KW, Sites SLM. A study of matched area
and personal airborne asbestos samples: evaluation for relationship and
distribution. Indoor-Built Environ 2000;9:192-200.
(6) Linch AL, Weist EG, Carter MD. Evaluation of tetraethyl lead
exposure by personal monitoring surveys. Am Ind Hyg Assoc J 1970;31:170-179.
(7) Lange JH. A statistical evaluation of asbestos air concentrations. Indoor-Built Environ 1999;8:293-303.
(8) Lange JH, Lange PR, Reinhard TK, Thomulka KW. A study of personal
and area airborne asbestos concentrations during asbestos abatement: a
statistical evaluation of fibre concentration data. Ann Occup Hyg 1996;40:449-466.
(9) Sherwood RJ. On the interpretation of air sampling for radioactive
particles. Am J Ind Hyg Assoc 1966;32:840-6.
(10) Seixas NS, Heyer NJ, Welp HAE, Checkoway H. Quantification of
historical dust exposures in the diatomaceous earth industry. Ann Occup
Hyg 1997;41:591-604.
(11) Purdham JT, Bozek PR, Sass-Korsak A. The evaluation of exposure of printing trade employees to polycyclic aromatic hydrocarbons. Ann Occup Hyg 1993;37:35-44.
(12) Corn M. Assessment and control of environmental exposure. J Allergy Clin Immunol 1983;72:231-241.
(13) Leidel NA, Busch KA, Lynch JR Occupational exposure sampling strategy manual. DEHW (NIOSH) Publication Number 77-173, National
Technical Information Service Number PB-274-792. Cincinnati, Ohio:
National Institute for Occupational Safety and Health, 1977.
(14) Harrison RM, Thornton CA, Lawrence RG, Mark D, Kinneisley RP, Ayres JG. Personal exposure monitoring of particulate matter, nitrogen dioxide, and carbon monoxide, including susceptible groups. Occup Environ Med 2002;59:671-9.
(15) Kromhout H, van Tongeren M. How important is personal exposure assessment in the epidemiology of air pollutants? Occup Environ Med 2003;60:143-144.
(16) Lange JH, Thomulka KW. Air sampling during asbestos abatement of floor tile and mastic. Bull Environ Cont Tox 2000;64:497-501.
(17) Sarin PS. Use of personal exposure modeling in risk assessment of air pollutants [electronic response to Kromhout H and van Tongeren M How important is personal exposure assessment in the epidemiology of air pollutants?]
occenvmed.com 2003http://oem.bmjjournals.com/cgi/eletters/60/2/143-a#68
The paper from Harrison and his co-workers [1] and the subsequent correspondence by Lange and others [2,3] has
re-ignited a debate about the relationship between personal and static sample measurements that started more than 40 years ago.
In 1957, the personal sampling pump had just been invented by Jerry Sherwood and Don Greenhalgh from the UK Atomic Energy Authority.[4] They compared their new persona...
The paper from Harrison and his co-workers [1] and the subsequent correspondence by Lange and others [2,3] has
re-ignited a debate about the relationship between personal and static sample measurements that started more than 40 years ago.
In 1957, the personal sampling pump had just been invented by Jerry Sherwood and Don Greenhalgh from the UK Atomic Energy Authority.[4] They compared their new personal sampler with the conventional static sampler and showed that personal exposures were generally higher than those made at a fixed location. This classic paper has recently been reproduced in the electronic edition of the Annals of Occupational Hygiene along with a commentary on its significance to the science of human exposure assessment.[5] In this commentary information concerning personal and static measurement results from papers published in that journal over that last ten years was reviewed. This showed, as Lange asserts in his letter to this journal,[3] that “personal samples are generally higher in concentration than static samples”. In this analysis more than 80% of the personal measurements exceeded the corresponding static sample concentration. The median ratio between personal and static concentrations was 1.5, although the individual data points ranged from 0.4 to 10. It is reasonable to expect that in general personal exposure would be greater than static samples if on average workers spend a proportion of their time close to sources of the hazardous substance.
Lange poses the question "are personal and static samples related?".[3] The answer must be "yes", but perhaps a more
pertinent question is: how can the relationship between personal and static samples be useful in epidemiological studies or risk evaluations? A simple conceptual model (shown in figure 1 below), is sufficient to convince us that there must be a relationship between personal and static monitoring data. The model comprises four air compartments and one for surfaces, all of which are interlinked by transfer processes. The air compartments represent the local external environment, room air (where static samples are obtained), breathing zone air (where personal air samples are collected) and the inhalation of contaminants into the nose or mouth. Note, a key assumption here is that the contaminant is thoroughly mixed throughout each compartment. In addition, in the model we have the potential for airborne contaminants to adsorb or sediment onto room surfaces and for this contamination to become re-suspended in the air. In general there is the potential for contaminants to be exchanged to and from each compartment, for example as air flows from the breathing zone to the body of the room it is replaced by air from the room. The purpose of showing this model is to illustrate the complexity of the processes relating room and breathing zone air concentrations and this is almost certainly the main reason why there is such a wide range in the ratio of personal and static air concentrations. Key factors in determining the relationship between personal and static measurements in any situation will include the volume of the room, the quantity of general ventilation, the time the person spends in the proximity of sources of hazardous substances (i.e. with a source in their breathing zone), the presence of other internal or environmental sources of the contaminant and others. In most circumstances, without knowing something about each of these factors it is impossible to predict what the relationship between personal and static concentrations might be.
There is one class of situations where room samples and personal samples are likely to be very similar. Using a simple mathematical model Cherrie[6] showed that in small poorly ventilated rooms it makes little difference whether the concentration is measured in the breathing zone compartment or in the room compartment because the contaminant quickly mixes throughout both spaces. In most domestic situations it is likely that this is the case since the rooms are generally small and the ventilation rate is likely to be low, probably less than one air-change per hour. Therefore, I think almost uniquely, in epidemiological studies where we want to assess the exposure of people in houses it probably does not make a lot of difference whether we use samplers located in the room or samplers located in the persons breathing zone. This will mostly not be the case in occupational epidemiological studies, where spaces are typically larger and ventilation rates greater.
references
(1) Harrison RM, Thornton CA, Lawrence RG et al. Personal exposure monitoring of particulate matter, nitrogen dioxide, and carbon monoxide, including susceptible groups. Occup Environ Med 2002;59:671-9.
(2) Kromhout H, van Tongeren M. How important is personal exposure assessment in the epidemiology of air pollutants? (letter) Occup Environ Med 2003;60:143.
(3) Lange JH. Are personal and static samples related? (letter) Occup Environ Med 2003; 60: 224-5.
(4) Sherwood RJ, Greenhalgh DMS. A personal air sampler. Ann Occup Hyg 1960; 2:127-32.
(5) Cherrie JW. The beginning of the science underpinning occupational hygiene. Ann Occup Hyg 2003; 47: 179-85.
(6) Cherrie JW. The effect of room size and general ventilation on the relationship between near and far-field concentrations. Appl Env Occup Hyg 1999; 14: 539-46.
Kromhout and van Tangeren [1] raise important issues regarding the
papers by Cherrie [2] and Harrison et al.[3] The major shortcomings of
the paper by Harrison et al.[3] are the small size of the sample (6
subjects each) used in the extrapolation of results. The three groups
studied were the children, elderly and subjects with preexisting disease.
The sample size in the disease categor...
Kromhout and van Tangeren [1] raise important issues regarding the
papers by Cherrie [2] and Harrison et al.[3] The major shortcomings of
the paper by Harrison et al.[3] are the small size of the sample (6
subjects each) used in the extrapolation of results. The three groups
studied were the children, elderly and subjects with preexisting disease.
The sample size in the disease category used only 2 subjects each with
chronic obstructive pulmonary disease (COPD), left ventricular failure
(LVF) and severe asthma. These sample sizes are rather inadequate to draw
any correlation. Thus the paper by Harrison et al.[3] does not adequately
represent generalized level of exposure of the individuals to carbon
monoxide (CO), nitrogen dioxide (NO2) and particulate matter (PM10).
In risk assessment of ill-health association with air contaminants,
uniform sampling of the pollutants at home, school, work and outdoor
activities is important. In a recent article [4] detailing the effect of
World Trade Center collapse, the authors emphasize that environmental
monitoring for exposure assessment is a complex technical task that
involves selection of pollutants for monitoring, location of monitors,
sample collection methods, risk assessment standards, sampling results and
data analysis. For example, the initial approach to the environmental
sampling at the World Trade Center [4] was to locate monitors at the
perimeter of the site, at locations where emergency and debris carrying
vehicles were leaving the site, on the debris pile, and at locations in
the surrounding community. Additional monitors were set up in the
community to ensure a safer environment for workers and students returning
to workplaces, homes and schools. Approximately, 66,000 results were
entered in a database collected between September 11 to November 13 for
subsequent analysis. Substances monitored included asbestos, particulate
matter (PM2.5 and PM10), dioxins, PCBs, CO, heavy metals and volatile
organic compounds (VOCs).
As pointed out by Schneider [5] deterministic models are developed
from equations based on mathematical principles, while statistical models
are developed by fitting to observed data.[6] In the statistical modeling
of inhalation exposure, mixed effect models have been useful. Linear Mixed
Effects Model with AR-1 autoregressive correlation structures has recently
been used by Levy et al.[7,8] in their studies.
For example, due to the difficulties in the measurement of personal
exposure, data on air pollution patterns in homogenous microenvironments
linked with activity data are often used as surrogates (7). In these
studies [7] PM2.5 indoor-outdoor ratios were found to be greater than1 in
settings with high levels of human activity. Cooking activities
contributed significantly to elevation in levels of PM2.5 along with other
pollutants. Using Linear Mixed Effects Models with AR-1 autoregressive
correlation structures, 10 minute average outdoor concentrations were
generally weak predictors of indoor levels.
As mentioned by Levy et al.[8] although ambient particulate matter
has been associated with ill-health, the health risks for individuals
depend in part on their daily activities. Information about levels of PM
size distributions in indoor and outdoor microenvironments can help
identify high-risk individuals. The authors used Linear Mixed Effects
Models with an AR-1 autoregressive correlation structure to evaluate
statistical significance of differences between microenvironments. Levels
of larger particles were generally higher near significant human activity,
and levels of smaller particles were higher near combustion sources. The
indoor PM10 concentrations were reported to be significantly higher than
the outdoors on buses and trolleys. Statistical models showed significant
variability among some indoor microenvironments.
As pointed out by Chang et al.[9] simulation of activities performed
by 65+ year olds indicate substantial variability in personal exposures of
PM2.5, O3, CO and VOCs over a 12-hour period. For example, one hour
personal CO exposures measured in vehicles were significantly higher than
those measured in other microenvironments and the correlation between
personal PM2.5 exposures and ambient concentrations was lowest in the
winter months for indoor non-residential microenvironment and highest in
vehicle microenvironments.
Thus the conclusions drawn by Harrison et al. [3] from the data on a
relatively small sample of subjects utilizing microenvironment modeling of
CO, NO2 and PM may not adequately reflect the overall exposure patterns.
The variance observed between measured and modeled values for PM10 among
elderly, COPD and children could be minimized by taking measurements in a
larger sample both indoors and outdoors and during summer and winter
months.
References
(1) Kromhout H, van Tongeren M. How important is personal exposure
assessment in the epidemilogy of air pollutants? Occup Environ Med 2003;
60: 143-144.
(2) Cherrie JW. How important is personal exposure assessment in the
epidemiology of air pollutants? Occup Environ Med 2002; 59: 653-654.
(3) Harrison RM, Thornton CA, Lawrence RG, Mark D, Kinnersley RP,
Ayres JG. Personal exposure monitoring of particulate matter, nitrogen
dioxide, and carbon monoxide, including susceptible groups. Occup Environ
Med 2002; 59: 671-679.
(4) Holtz TH, Leighton J, Balter S, Weiss D, Blank S, Weisfuse I, in
Levy BS, Sidel VW (Eds). Terrorism and Public Health. A balanced approach
to strengthening systems and protecting people Oxford University Press,
Inc., Oxford, 2003, pp.19-48.
(5) Schneider T. Improving exposure assessment requires measurements
and modeling. Scand J Work Environ Health 2002; 28: 367-369.
(6) Hornung RW, Griefe AL, Stayner LT, Steenland NK, Herrick RF,
Elliott LJ et al. Statistical model for prediction of retrospective
exposure to ethylene oxide in occupational mortality study. Am J Ind Med 1994; 25:825-836.
(7) Levy JI, Dumyahn T, Spengler JD. Particulate matter and polycyclic
aromatic hydrocarbon concentrations in indoor and outdoor
microenvironments in Boston, Massachusetts. J Expo Anal Environ Epidemiol 2002; 12: 104-114.
(8) Levy JI, Houseman EA, Ryan L, Richardson D, Spengler JD. Particle
concentrations in urban microenvironments. Environ Health Perspect 2000; 108:1051-1057
(9) Chang LT, Koutrakis P, Catalano PJ, Suh HH. Hourly personal
exposures to fine particles and gaseous pollutants-results from Baltimore,
Maryland. J Air Waste Manag Assoc 2000; 50: 1223-1235.
Although at least 455 million people worldwide live within potential
exposure range of a volcano active within recorded history,[1]
surprisingly little primary epidemiological research on health effects of
volcanic emissions has been published. The research by Forbes et al.[2] on
the respiratory effects of the eruptions in Montserrat is therefore very
welcome. However, more studies are neede...
Although at least 455 million people worldwide live within potential
exposure range of a volcano active within recorded history,[1]
surprisingly little primary epidemiological research on health effects of
volcanic emissions has been published. The research by Forbes et al.[2] on
the respiratory effects of the eruptions in Montserrat is therefore very
welcome. However, more studies are needed to determine the
transferability of results to volcanic emissions elsewhere. There may be
important differences between volcanoes and between events from the same
volcano in terms of eruption pattern, gaseous emissions, base composition
of ash (e.g. cristobalite concentrations), compounds adsorbed onto ash
particles (which may be volcanic in origin or derived from other pollution
sources), the percentage of particles small enough to be respirable and
toxicological activity.[3] For example, most respirable ash in Montserrat
has originated from pyroclastic flows, with cristobalite concentrations
measured at 20.1%, but Montserrat ash derived from phreatic explosions has
lower cristobalite concentrations (8.6%)[4] and these are higher than the
4.2% quoted for ash from the United States Mount St Helens eruptions in
1980.[5] The Soufriere Hills volcano in Montserrat has produced unusually
frequent pyroclastic flows, resulting in high exposures to fine ash even
in residential areas distant from the volcano but population exposure to
volcanic gases such as sulphur dioxide has been low. This contrasts with
volcanoes such as Sakurajima, Japan where frequent ashfalls have been
accompanied by SO2 emissions[6] or Kilauea, Hawaii where emissions are
predominantly SO2.[7]
Studies of health effects of volcanic ash exposure may help elucidate
mechanisms relevant to action of anthropogenic pollution. For example, it
remains unclear whether concentration or composition of anthropogenic
particulate air pollution is more important for respiratory health
effects.[8] Montserrat children demonstrated increased levels of wheeze
and bronchial hyperreactivity following repeated exposures to high
concentrations of respirable dust, with elevated cristobalite content but
low soluble acid content and low in vitro[9] and in vivo[4] bioreactivity
in toxicological studies. Long-term exposure to high levels of
cristobalite might be expected to be associated with reductions in lung
volumes, not presented in this study, rather than with increased bronchial
reactivity. This raises the possibility that the effect of Montserrat ash
on bronchial reactivity may have been related to the quantity rather than
the quality of the particulates.
Finally, it is unclear whether a peak flow meter or hand-held
spirometer was used in the Montserrat study. A hand-held spirometer is
suggested as the ideal measuring tool for field investigations into
respiratory effects of volcanic emissions in children. It can be used
reliably in children as young as 5 years, gives a range of readings
including FEV1, which has better baseline reproducibility than peak
flow[10] and lung volumes, which may be particularly useful if follow-up
studies into long-term effects are planned.
References
(1) Small D, Naumann T. The global distribution of human population
and recent volcanism. Environmental Hazards 2001; 3:93-109.
[2] Forbes L, Jarvis D, Potts J, Baxter PJ. Volcanic ash and respiratory
symptoms in children in the island of Montserrat, British West Indies.
Occup Environ Med 2003; 60:207-211.
[3] Vallyathan V, Robinson V. Comparative in vitro cytotoxicity of
volcanic ashes from Mount St. Helens, El Chichón, and Galunggung. Journal
of Toxicology and Environmental Health 1984; 14:641-654.
[4] Housley DG, Berube KA, Jones TP et al. Pulmonary epithelial response
in the rat lung to instilled Montserrat respirable dusts and their major
mineral components. Occup Environ Med 2002; 59(7):466-472.
[5] Baxter PJ, Bonadonna C, Dupree R et al. Cristobalite in volcanic ash
of the Soufriere Hills Volcano, Montserrat, British West Indies. Science
1999; 283:1142-1145.
[6] Uda H, Akiba S, Hatano H, Shinkura R. Asthma-Like Disease in the
Children Living in the Neighborhood of Mt. Sakurajima. Journal of
Epidemiology 1999; 9(1):27-31.
[7] Mannino DM, Ruben S, Holschuh FC et al. Emergency Department Visits
and Hospitalizations for Respiratory Disease on the Island of Hawaii, 1981
to 1991. Hawaii Medical Journal 1996; 55(March):48-54.
[8] Peden DB. Pollutants and asthma: role of air toxics. Environ Health
Persp 2002; 110(Suppl 4):565-568.
[9] Wilson MR, Stone V, Cullen RT et al. In vitro toxicology of respirable
Montserrat volcanic ash. Occup Environ Med 2000; 57:727-733.
[10] Malmberg LP, Nikander K, Pelkonen AS et al. Acceptability,
reproducibility and sensitivity of forced expiratory volumes and peak
expiratory flow during bronchial challenge testing in asthmatic children.
Chest 2001; 120(6):1843-1849.
The scientific literature is full of of papers and ideas giving
hypothesis. This was the objective of our letter. As it is stated at the
end, we do not know if the finding is consistent or due to chance. We
think that there are reasons pointing that our findings could have a solid
fundament;
1) There were no musicians among the controls, 2) the musicians
among the cases were win...
The scientific literature is full of of papers and ideas giving
hypothesis. This was the objective of our letter. As it is stated at the
end, we do not know if the finding is consistent or due to chance. We
think that there are reasons pointing that our findings could have a solid
fundament;
1) There were no musicians among the controls, 2) the musicians
among the cases were wind musicians and, 3) the proportion of musicians in
our region is extremely low.
It should be noted that we do not give any
numeric estimation because it is not practical. As Dr Geis says, precisely
the fact that there were no wind musicians among the controls reinforce
our hypothesis, although confusion by smoking status can not be excluded.
Since tobacco is responsible of around 85-90% of all lung cancers, only
studies including never-smokers are completely free of confusion and then
only this type of study, following the point of view of Dr Geis, could
prove our hypothesis.
How is it significant that two ex-smokers got lung cancer - whether or
not they played wind instruments? Were these musicians the only ex-smokers
of the 130+ lung cancer sufferers? Did/do these musicians play in smoke-
filled bars?
With no wind instrument musicians in the control group and the
confounding factor of being ex-smokers, the authors certainly should have
provided better reason for...
How is it significant that two ex-smokers got lung cancer - whether or
not they played wind instruments? Were these musicians the only ex-smokers
of the 130+ lung cancer sufferers? Did/do these musicians play in smoke-
filled bars?
With no wind instrument musicians in the control group and the
confounding factor of being ex-smokers, the authors certainly should have
provided better reason for their facile association of lung cancer with
the playing of wind instruments - at least as much as their imagined
mechanism.
The update of predictions of mortality from pleural mesothelioma in
the Netherlands [1] provides welcome news that the peak number and the
total during 2000-2028 is now predicted to be only a little more than half
of the figures predicted only four years earlie.[2] This marked change
in prediction has occurred because the known decrease in asbestos use
after 1984 and a ban in 1993 were taken into account...
The update of predictions of mortality from pleural mesothelioma in
the Netherlands [1] provides welcome news that the peak number and the
total during 2000-2028 is now predicted to be only a little more than half
of the figures predicted only four years earlie.[2] This marked change
in prediction has occurred because the known decrease in asbestos use
after 1984 and a ban in 1993 were taken into account in the modelling, and
there were five extra years of data (1994-98).
Since most mesotheliomas are caused by asbestos the pattern of use
during different periods of time has a marked influence on the risk in
cohorts whose working lives covered different periods. The marked effect
of the discontinuation of crocidolite importation by 1970 into the United
Kingdom on the amount of crocidolite found in the lungs of men, born in
1943 or later who developed a mesothelioma between 1990 and 1996 when aged
36 to 52 years,[3] was clear when compared with the lung contents of
mesotheliomas in 1976 and 1977.[4] The average amount of crocidolite in
the lungs of the men with mesothelioma in 1990-96 was about a tenth of
that in the lungs of the 1976-77 cases. This difference was a consequence
of the shorter period of exposure and the longer time since exposure
during which elimination of fibres occurred in the absence of new
exposure.
The importance of the effect of elimination is illustrated by results
from former workers at the Wittenoom crocidolite mine and mill in Western
Australia. Exposure of this group ceased in 1966 when the mine and mill
were closed. Based on an analysis of the number of deaths with
mesothelioma in men to the end of 1986, predictions were made of the
number occurring up to 2020.[5,6] The model of the mesothelioma death
rate used was that the rate increased with a power of time since exposure,
moderated by a factor representing elimination of crocidolite fibres over
time since exposure. Rates of elimination from zero to 15% per year were
considered. Assuming no elimination, which was the usual model used at
that time, predicted more than twice as many mesotheliomas by 2020 than an
elimination rate of 15% per year. Preliminary results to 1999 were given
by Musk et al,[7] and it is now known that the number of mesothelioma
deaths in men in the period 1987 to 2000 was similar to the lowest
predictions made based on the number up to 1986. This result is evidence
that models of mesothelioma incidence that take account of a gradual
elimination of crocidolite from the lungs after exposure are more
realistic. There is strong evidence from other sources that such
elimination does occur and that for crocidolite the rate of elimination is
in the range of 10 to 15% a year.[8]
There is a high continuing toll from the use of asbestos in Europe
and from the mining and milling of crocidolite at Wittenoom in Australia,
but fortunately recent evidence strongly suggests that the number of
mesotheliomas will not be as high as earlier predictions.
G. Berry 1, A.W. Musk 2,3, N.H. de Klerk 3,4, A. Johnson 5 and D.H.
Yates 5
Affiliations
1 School of Public Health, University of Sydney, New South Wales
2006, Australia 2 Sir Charles Gairdner Hospital, Nedlands, Western Australia 3 Department of Public Health, University of Western Australia 4 Centre for Child Health Research, University of Western Australia 5 Dust Diseases Board (NSW) Research and Education Unit, Sydney
References
(1) Segura O, Burdorf A, Looman C. Update of predictions of mortality
from pleural mesothelioma in the Netherlands. Occup Environ Med 2003; 60:
50-5.
(2) Peto J, Decarli A, La Vecchia C, Levi F, Negri E. The European
mesothelioma epidemic. Br J Cancer 1999; 79: 666-72.
(3) McDonald JC, Armstrong BG, Edwards CW, Gibbs AR, Lloyd HM, Pooley
FD, Ross DJ, Rudd RM. Case-referent survey of young adults with
mesothelioma: I. Lung fibre analyses. Annals of Occupational Hygiene
2001; 45(7): 513-8.
(4) Berry G. Asbestos lung fibre analysis in the United Kingdom.
Annals of Occupational Hygiene 2002; 46: 523-6.
(5) Berry G. Prediction of mesothelioma, lung cancer, and asbestosis
in former Wittenoom asbestos workers. Br J Ind Med 1991; 48: 793-802.
(6) de Klerk NH, Armstrong BK, Musk W, Hobbs MST. Predictions of
future cases of asbestos-related disease among former miners and millers
of crocidolite in Western Australia. Med J Aust 1989; 151: 616-20.
(7) Musk AW, de Klerk NH, Olsen NJ, Hansen J, Ambrosini GL, Fritschi
L, Merler E, Hobbs MST. Mortality in miners and millers of crocidolite in
Western Australia: follow-up to 1999. Ann occup Hyg 2002; 46 (Suppl 1): 90-2.
(8) Berry G. Models for mesothelioma incidence following exposure to
fibers in terms of timing and duration of exposure and the biopersistence
of the fibers. Inhal Toxicol 1999;11:111-30.
We would like to comment on the study by Flodin et al.[1] We
believe it has multiple methodological flaws and does not add to the
understanding of the relationship of exposure to trace concentrations of
waste anesthetic gases and the health of operating room workers.
First, the method of data collection, i.e, by an “appeal” (authors’
word)” in a trade journal for nurses for individ...
We would like to comment on the study by Flodin et al.[1] We
believe it has multiple methodological flaws and does not add to the
understanding of the relationship of exposure to trace concentrations of
waste anesthetic gases and the health of operating room workers.
First, the method of data collection, i.e, by an “appeal” (authors’
word)” in a trade journal for nurses for individuals with multiple
sclerosis to identify themselves is bound to result in responder bias.
Many of the early epidemiologic surveys examining the relationship of
exposure to waste anaesthetic gases and adverse health effects were
confounded by responder bias. An example of the problem was reported by
Axelsson and Rylander[2] who reviewed all histories in one survey which
claimed an increased risk of spontaneous abortion in nurse anaesthetists.
Medical records were examined to determine the occurrence of abortion.
When data from non- responders were included, there was no difference in
adverse effects between the groups.
Another major flaw in the study is that dosage of waste anaesthetic
gases to which nurse anaesthetists were exposed was not measured. In fact
it is not known if nurse anaesthetists actually were exposed as scavenging
of waste anaesthetic gases was implemented in operating rooms world-wide
during the period of the study. When scavenging systems are in place,
exposure to waste anaesthetic gases is minimal. Indeed, it is possible
that some of the nurses worked only in scavenged theaters. For the study
to have any relevance, exposure of affected (those with MS) and unaffected
nurses must be reported. Also lacking is information regarding the
number of air exchanges in the operating room where the nurses worked.
Another problem with the study is there is no reference to possible
confounding factors, such as exposure to other environmental pollutants
(tobacco smoke, methyl methacrylate from cement in orthopedic operating
rooms), radiation, cytotoxic drugs,[3] and other variables thought to affect
health, such as shift work and stress. If ill affects occurred, they may
not have been due to exposure to trace levels of waste anaesthetic gases.
Finally, the authors do no mention the studies that have reviewed the
epidemiologic data examining the purported link between exposure to trace
concentrations of waste anaesthetic gases and adverse health effects.
Analysis of these data by two independent groups of epidemiologists[4,5]
showed that the reported differences in adverse health affects were small
and within the range that might be due to bias or uncontrolled variables,
i.e, flaws in study design especially data collection and responder bias
as may have occurred in the study by Flodin et al.[1] More recently, a
mortality study[6] showed that there was no difference between
anesthesiologists and internists in death rates from chronic neurological
disease. Finally, Spence and Maran[7-10] carried out a prospective study in
the United Kingdom collecting health and anaesthetic exposure data from
11,500 female physicians aged 40 or less working in hospital practice.
They did not find an increased incidence of neurological problems related
to occupation.
In summary, we believe the conclusions in the report by Flodin et
al.1 are incorrect because they are based on flawed methodology. Its
publication has probably caused unnecessary anxiety in operating room
workers. By our letter, we hope to allay these concerns.
Diana G. McGregor, M.B.B.S., FRCA
Department of Anesthesiology
Mayo Clinic
Rochester, MN 55902
Richard I. Mazze, M.D.
Jeffrey M. Baden, M.B.B.S., FRCA, MRCP (UK)
Department of Anesthesiology
Stanford University
Stanford CA 94305
References
(1) Flodin U, Landtblom AM, Axelson O: Multiple sclerosis in nurse
anaesthetists. Occup Environ Med 2003;60: 66-8.
(2) Axelsson G, Rylander R: Exposure to anaesthetic gases and
spontaneous abortion: response bias in a postal questionnaire. Int J
Epidemiol 1982; 11: 250-256
(3) Hirst M, Tse S, Mills DG, Levin L, White DF: Occupational exposure
to cyclophosphamide. Lancet 1984; 1: 186-8.
(4) Buring JE, Hennekens CH, Mayrent SL, Rosner B, Greenberg ER,
Colton T: Health experiences of operating room personnel. Anesthesiology
1985; 62: 325-330
(5) Tannenbaum TN, Goldberg RJ: Exposure to anesthetic gases and
reproductive outcome. A review of the epidemiologic literature. J Occup
Med 1985; 27: 659-668
(6) Alexander BH, Checkoway H, Nagahama SI, Domino KB: Cause-specific
mortality risks of anesthesiologists. Anesthesiology 2000; 93: 922-30.
(7) Spence AA, Knill-Jones RP: Is there a health hazard in anaesthetic
practice? Br J Anaesth 1978; 50: 713-719
(8) Spence A. How safe is anesthesia for you and your patient?
Occupational risks of the operating room? Data from the U.K. ten year
prospective study. Bulletin of the New York State Postgraduate Assembly
1985; Dec: 140.
Dear Editor,
We read the letter from Dr Smith with interest and thank him for suggesting his paper for discussion. Dr Smith argued that (i) there was significant overlap between his study [1] and ours [2], and (ii) oxygen desaturation as measured by pulse oximetry was an inappropriate means for testing exercise desaturation. We strongly disagreed with both points.
(i) Our study and that of Smith and...
Dear Editor
The publication of "Radiographic (ILO) readings predict arterial oxygen desaturation during exercise in subjects with asbestosis" by YCG Lee et al. from the Sir Charles Gardiner Hospital in Perth [1] presents no new information and fails to reference an earlier paper on the same subject which included more patients with clinical asbestosis and four different control groups.[2] This paper actually m...
Dear Editor
The letter [1] by Professor Cherrie in this issue addresses the long-standing question as to whether static (area, stationary) samples can be used to estimate exposure to people in lieu of personal measurements for epidemiological investigations. In my previous letter [2] the question was ask “are personal and static samples related?” and Cherrie [1] answered this question as “yes”. As mentioned in my...
The paper from Harrison and his co-workers [1] and the subsequent correspondence by Lange and others [2,3] has re-ignited a debate about the relationship between personal and static sample measurements that started more than 40 years ago.
In 1957, the personal sampling pump had just been invented by Jerry Sherwood and Don Greenhalgh from the UK Atomic Energy Authority.[4] They compared their new persona...
Dear Editor
Kromhout and van Tangeren [1] raise important issues regarding the papers by Cherrie [2] and Harrison et al.[3] The major shortcomings of the paper by Harrison et al.[3] are the small size of the sample (6 subjects each) used in the extrapolation of results. The three groups studied were the children, elderly and subjects with preexisting disease. The sample size in the disease categor...
Dear Editor
Although at least 455 million people worldwide live within potential exposure range of a volcano active within recorded history,[1] surprisingly little primary epidemiological research on health effects of volcanic emissions has been published. The research by Forbes et al.[2] on the respiratory effects of the eruptions in Montserrat is therefore very welcome. However, more studies are neede...
Dear Editor
The scientific literature is full of of papers and ideas giving hypothesis. This was the objective of our letter. As it is stated at the end, we do not know if the finding is consistent or due to chance. We think that there are reasons pointing that our findings could have a solid fundament;
1) There were no musicians among the controls,
2) the musicians among the cases were win...
Dear Editor
How is it significant that two ex-smokers got lung cancer - whether or not they played wind instruments? Were these musicians the only ex-smokers of the 130+ lung cancer sufferers? Did/do these musicians play in smoke- filled bars?
With no wind instrument musicians in the control group and the confounding factor of being ex-smokers, the authors certainly should have provided better reason for...
Dear Editor
The update of predictions of mortality from pleural mesothelioma in the Netherlands [1] provides welcome news that the peak number and the total during 2000-2028 is now predicted to be only a little more than half of the figures predicted only four years earlie.[2] This marked change in prediction has occurred because the known decrease in asbestos use after 1984 and a ban in 1993 were taken into account...
Dear Editor
We would like to comment on the study by Flodin et al.[1] We believe it has multiple methodological flaws and does not add to the understanding of the relationship of exposure to trace concentrations of waste anesthetic gases and the health of operating room workers.
First, the method of data collection, i.e, by an “appeal” (authors’ word)” in a trade journal for nurses for individ...
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