We thank Dr. Kawada for his interest in our manuscript entitled
"Associations of low-level urine cadmium with kidney function in lead
workers."[1] As discussed in the methods and shown in the footnotes to
Tables 3 and 4 in the manuscript, we adjusted for blood and tibia lead. We
have presented lead analyses in this cohort in multiple past
publications[2-8] so, in order to focus on the unique cadmium associations
and compl...
We thank Dr. Kawada for his interest in our manuscript entitled
"Associations of low-level urine cadmium with kidney function in lead
workers."[1] As discussed in the methods and shown in the footnotes to
Tables 3 and 4 in the manuscript, we adjusted for blood and tibia lead. We
have presented lead analyses in this cohort in multiple past
publications[2-8] so, in order to focus on the unique cadmium associations
and comply with space considerations, we did not show the lead regression
coefficients. Multiple linear regression was used in the analysis.
References:
1 Weaver VM, Kim NS, Jaar BG et al. Associations of low-level urine
cadmium with kidney function in lead workers. Occup Environ Med
2011;68:250-256. doi:oem.2010.056077 [pii]
10.1136/oem.2010.056077 [doi] [published Online First 2010/10/27].
2 Weaver VM, Lee BK, Ahn KD et al. Associations of lead biomarkers
with renal function in Korean lead workers. Occup Environ Med 2003;60:551-
62. 2003/07/29].
3 Weaver VM, Schwartz BS, Ahn KD et al. Associations of renal
function with polymorphisms in the delta-aminolevulinic acid dehydratase,
vitamin D receptor, and nitric oxide synthase genes in Korean lead
workers. Environ Health Perspect 2003;111:1613-9. 2003/10/07].
4 Weaver VM, Jaar BG, Schwartz BS et al. Associations among lead dose
biomarkers, uric acid, and renal function in Korean lead workers. Environ
Health Perspect 2005;113:36-42. 2005/01/01].
5 Weaver VM, Lee BK, Todd AC et al. Associations of patella lead and
other lead biomarkers with renal function in lead workers. J Occup Environ
Med 2005;47:235-43. doi:00043764-200503000-00005 [pii] [published Online
First 2005/03/12].
6 Weaver VM, Schwartz BS, Jaar BG et al. Associations of uric acid
with polymorphisms in the delta-aminolevulinic acid dehydratase, vitamin D
receptor, and nitric oxide synthase genes in Korean lead workers. Environ
Health Perspect 2005;113:1509-15. 2005/11/03].
7 Weaver VM, Lee BK, Todd AC et al. Effect modification by delta-
aminolevulinic acid dehydratase, vitamin D receptor, and nitric oxide
synthase gene polymorphisms on associations between patella lead and renal
function in lead workers. Environ Res 2006;102:61-9. doi:S0013-
9351(06)00002-8 [pii]
10.1016/j.envres.2006.01.001 [doi] [published Online First 2006/02/21].
8 Weaver VM, Griswold M, Todd AC et al. Longitudinal associations
between lead dose and renal function in lead workers. Environ Res
2009;109:101-7. doi:S0013-9351(08)00215-6 [pii]
10.1016/j.envres.2008.09.005 [doi] [published Online First 2008/11/29].
As it had been discussed in the study[1], selection bias may affect
the validity of the result. In this case there would be selection bias, if
the response rate in the survey associated with occupation, and the
distribution of occupation among controls did not reflect that among the
general population. However, if the response rate was independent from
occupations, health status, other lifestyle, se...
As it had been discussed in the study[1], selection bias may affect
the validity of the result. In this case there would be selection bias, if
the response rate in the survey associated with occupation, and the
distribution of occupation among controls did not reflect that among the
general population. However, if the response rate was independent from
occupations, health status, other lifestyle, selection bias may not exist
regardless the response rate. An addition survey only requires information
on occupation, sex and age might be able to evaluate the strength of
selection bias among the controls. Or it would be great if there were any
comparable official statistic .
Reference
1. Mester, B., et al., Occupation and malignant lymphoma: a
population based case control study in Germany. Occup Environ Med, 2006.
63(1): p.17-26.
This article recalls a controversy of the early 1930s, when the
authority of no less a genius than Professor JS Haldane was challenged on
behalf of South Wales coalminers by a mining mineralogist W. R. Jones, who
as a consequence was to acquire the soubriquet "Sericite". [1]
Their disease was considered by Haldane not to be attributable to the
dust to which they were exposed, as its level of c...
This article recalls a controversy of the early 1930s, when the
authority of no less a genius than Professor JS Haldane was challenged on
behalf of South Wales coalminers by a mining mineralogist W. R. Jones, who
as a consequence was to acquire the soubriquet "Sericite". [1]
Their disease was considered by Haldane not to be attributable to the
dust to which they were exposed, as its level of crystalline silica was
too low: further, it was claimed that coal mine dust reduced the risks of
tuberculosis, and promoted longevity.
Jones' hypothesis was that much of the respiratory disease incurred
in such dusty industries as coal mining, gold mining, and pottery, was
related to the cericite rather than to the crystalline silica content of
their dusts. There were fallacies in the scientific arguments on both
sides, but in the event sentiment sided with Jones, and the miners
received compensation. Algranti et al confirm that yet another non-
asbestos mineral fibre can be biologically active even when below the
length that most hygienists care to be concerned about.
References
[1] Greenberg M. 'A battle for compensation for Welsh coal miners: JS
Haldane v "Sericite" Jones, 1932-1934..' Am J Ind Med, 1997;32: 309-314.
High temperatures and mortality - even more relevant in desert
environments.
Your editorial on exposure to high ambient temperatures and mortality
is timely [1]. The Gasparrini et al.[2] paper on ambient air temperatures
and mortality in temperate England and Wales provides further support for
population-level preventive measures to reduce the likelihood of adverse
health effects from elev...
High temperatures and mortality - even more relevant in desert
environments.
Your editorial on exposure to high ambient temperatures and mortality
is timely [1]. The Gasparrini et al.[2] paper on ambient air temperatures
and mortality in temperate England and Wales provides further support for
population-level preventive measures to reduce the likelihood of adverse
health effects from elevated environmental temperatures.
The risk of heat-related illness and death is especially relevant to
desert environments, such as in the United Arab Emirates (UAE), where
summer temperatures can often exceed 50 degrees Celsius. In recent years,
the risk of morbidity and mortality from heat exposure was compounded when
the holy month of Ramadan coincided with summer in the Middle East. During
Ramadan, Muslims abstain from consuming fluids or food during daylight
hours. Additional risk factors for these workers are prolonged day shifts,
strenuous outdoor manual work and inadequate rest breaks. Muslim workers
constitute a majority of the expatriate workforce in several Middle
Eastern countries. Preventive measures to reduce the likelihood of
morbidity and/or mortality in this group are particularly pertinent over
the next few years when Ramadan will again fall during summer. In the UAE,
the Health Authority of Abu Dhabi developed a "Safety in the Heat"
campaign which distributed educational materials in five different
languages to over 800,000 outdoor workers focusing on self-monitoring
hydration status using urine colour, adequate hydration before and after
fasting, and self-pacing strategies whilst performing physical activity
[3]. An environmental early warning system could be developed using a
composite index of thermal stress incorporating several environmental
parameters (i.e. dry bulb temperature, wet bulb temperature, wind speed
and radiant heat). Another index is the Thermal Work Limit [4] which is a
good indicator of heat stress in outdoor workers and would be a useful
addendum to the Department of Health's Heatwave environmental monitoring
plan [5].
1. Ebi KL. High temperatures and cause-specific mortality. Occup
Environ Med 2012;69:3-4.
2. Gasparrini A, Armstrong B, Kovats S, Wilkinson P. The effect of
high temperatures on cause-specific mortality in England and Wales. Occup
Environ Med 2012;69:56-61.
3. Joubert D, Thomsen J, Harrison O. Safety in the Heat: A
Comprehensive Program for Prevention of Heat Illness Among Workers in Abu
Dhabi, United Arab Emirates, Am J Public Hlth 2011;101(3):395-398.
4. Brake DJ, Bates GP. Limiting metabolic rate (Thermal Work Limit)
as an Index of Thermal Stress. App Occup Environ Hyg 2002;17(3):176-186.
5. Department of Health. Heatwave: Plan for England - Protecting
Health and Reducing Harm From Extreme Heat and Heatwave. London:
Department of Health, 2009.
Editor,
I was interested to read the excellent COPE Report Paper[1] and note
Occupational and Environmental Medicine's intention to follow these
guidelines.
In particular, from the occupational health point of view, I welcome
the inclusion of involvement of the study participants in consideration
and agreement of the research protocol, though I am a little sad that the
COPE Committee...
Editor,
I was interested to read the excellent COPE Report Paper[1] and note
Occupational and Environmental Medicine's intention to follow these
guidelines.
In particular, from the occupational health point of view, I welcome
the inclusion of involvement of the study participants in consideration
and agreement of the research protocol, though I am a little sad that the
COPE Committee have restricted their consideration of pre-publication
information of the results to "patients, especially if there are clinical
implications."[1]
As you are aware, the Professional Guidance on Ethics for
Occupational Physicians[2] now includes a specific section on occupational
health research which highlights the need to consider release of results,
including pre-publication briefings to workforces who are the subjects of
such research. I know that the BMJ Publishing Group have long been in
support of this sort of ethical stance, and would hope that in the future
COPE might expand their consideration of pre-publication information
beyond patients and clinical medicine into workers in the occupational
setting.
Another area of ethics of research relevant to occupational health
not considered by COPE is the field of data access and shared data.
Research in the work place can be consented to by the workforce for a
specific purpose, specific protocol, and even on occasion for a specific
researcher's use. There remains the question whether this data once
obtained is, or should be, available for others to use in other protocols
for other purposes. Certainly in the nuclear industry, we have taken the
view that it should not without revisiting the consent of the workforce.
Perhaps this too is an area that COPE might address in the future.
References
1. Committee on Publication Ethics. Occup Environ Med 2000;57:506-9.
2. Faculty of Occupational Medicine. Section 6. Guidance on Ethics for Occupational Physicians. 5th ed. London: Faculty of Occupational Medicine, 1999.
We read with interest a recently published study on personal exposure
of asthmatic children to nitrogen dioxide (NO2), relative to
concentrations in outdoor air.[1]
In their results, authors didn't find:
1. "…significant correlation… between each child's weekly mean personal
exposures and mean outdoor concentrations for the corresponding periods";
2. "…marked evidence of seasonality" on personal exposure...
We read with interest a recently published study on personal exposure
of asthmatic children to nitrogen dioxide (NO2), relative to
concentrations in outdoor air.[1]
In their results, authors didn't find:
1. "…significant correlation… between each child's weekly mean personal
exposures and mean outdoor concentrations for the corresponding periods";
2. "…marked evidence of seasonality" on personal exposure .
They concluded: "…at low concentrations, changes in NO2 in outdoor
air…contribute little to variations in personal exposure to the
pollutant."
We think that these conclusions cannot be drawn from the method used to
evaluate outdoor concentrations. Besides, we report different findings on
seasonal trend at higher levels of personal exposure.
We performed a study to evaluate the annual distribution of personal
exposure to NO2 in school children of Novara, a small city in north west
Italy (about 110.000 inhabitants) and to study determinants of this
exposure.
NO2 exposure was measured using passive samplers (Palme's tubes) in 310
school children aged 5-14 years. The children wore the tubes 5 days a
week, in each season of the year.
The possible differences in personal measurements were assessed by ANOVA
and Tuckey tests. Information about the sources of potential exposure was
collected by a questionnaire. The relative risk for these variables was
estimated with a multiple regression model (Logit). The annual average of
6,200 measurements was 42.7 mg/m3 with a significant difference between
seasons, and higher values in winter. The only factor associated with
increased personal exposure was to live along busy streets, only for
children of maternal school.
Even if designs of two studies are different, at this point it is possible
to make some considerations.
Firstly, at higher levels of NO2 exposure respect to those reported by
Linaker et al,[1] the seasonal changes of concentration in outdoor air
contribute significantly to variations in intra-individual exposure.
Besides, the role of risk factors present at home, respect to child-child
differences, is not clear. We suppose that our result depends on actual
habit of children to spend, everyday, a lot of hours in many different
occupations away from home, reducing the individual differences caused by
domestic sources of NO2.
Secondly, we think that only one measurement station used by Linaker et
al.[1] is inappropriate to evaluate the real impact of outdoor
concentrations on personal exposure, because outdoor levels of pollutants
are, in our and in other studies,[2] [3] related to traffic density in
each street.
1. Catherine H Linaker, Anoop J Chauhan, Hazel M Inskip, Stephen T
Holgate. Personal exposure of children to nitrogen dioxide relative to
concentrations in outdoor air; Occup Environ Med 2000;57:472-6.
2. Shima M, Adachi M. Indoor nitrogen dioxide in homes along trunk roads
with heavy traffic; Occup Environ Med 1998;55:428-33.
3. Kramer U, Koch T, Ranft U, Ring J, Behrendt II. Traffic related air
pollution is associated with atopy in children living in urban areas;
Epidemiology 2000;11:64-70.
Cesaroni et al make an assessment of the health benefits of a traffic management scheme in Rome based on changes in vehicle emissions and associated chronic risk factors(1). The authors estimate that a combination of the policy intervention and unrelated fleet changes caused a 38% reduction in the annual mean exposure of NO2 and a 29% reduction of PM10 within the 'railway ring' restricted zone bet...
Cesaroni et al make an assessment of the health benefits of a traffic management scheme in Rome based on changes in vehicle emissions and associated chronic risk factors(1). The authors estimate that a combination of the policy intervention and unrelated fleet changes caused a 38% reduction in the annual mean exposure of NO2 and a 29% reduction of PM10 within the 'railway ring' restricted zone between 2001 and 2005. The majority of this decrease was unrelated to the intervention, however, NO2 reductions specifically driven by the policy, were translated to 1387 years of life gained per 100,000 residents.
We strongly believe that such statements based solely on modelled and hence theoretical decreases in pollution require validation using empirical data. Measurements from the European Environment Agency's air quality database(2) show that measured annual mean NO2 concentrations within the 'railway ring' zone actually increased between 2001 and 2005 (80 ug/m3 to 82 ug/m3 at roadside site IT0946A and 39 ug/m3 to 41 ug/m3 at background site IT0953A). It is therefore evident that the assumptions used in the analysis did not reflect real world conditions.
Similarly, in studying the impacts of the London Congestion Charging Scheme, Kelly et al, found little evidence of a beneficial effect on monitored concentrations of NO2 and PM10, despite a large and sustained reduction in vehicle numbers(3). This was attributed to the relatively small area of the zone and an increase in the proportion of the vehicle fleet using diesel engines. It is also now widely accepted that the Euro emission standards are not delivering the predicted reductions in NOX(4).
While theoretical estimations of the health benefits of policy interventions are welcome, care should be taken to validate these estimates with empirical measurements wherever possible as man and machine rarely behave as predicted.
References:
1 Cesaroni G, Boogaard H, Jonkers S, Porta D, Badaloni C, Cattani G, Forastiere F, Hoek G. Health benefits of traffic-related air pollution reduction in different socioeconomic groups: the effect of low-emission zoning in Rome. Occup Environ Med. 2012;69(2):133-9.
3 Kelly F.J., Anderson H.R., Armstrong B., Atkinson R, Barratt B., Beevers S.D, Derwent D., Green D., Mudway I., Wilkinson P., 2011. The Impact of the Congestion Charging Scheme on Air Quality in London. Research Report Number 155. Health Effects Institute, Boston, MA, USA. April 2011. Available from http://pubs.healtheffects.org/types.php?type=1.
4 Carslaw D.C., Beevers S.D., Westmoreland E., Williams W., Tate J., Murrells T., Stedman J., Li Y., Grice S., Kent A., Tsagatakis I., 2011. Trends in NOX and NO2 emissions and ambient measurements in the UK. Report for Defra, March 2011. Available from http://uk-air.defra.gov.uk/library/reports?report_id=645.
We read with interest the paper on glutaraldehyde and symptoms in
endoscopy nursing staff.[1] It is reported that there was an absence of
objective evidence of the physiological changes associated with asthma.
Peak expiratory flow (PEF) records from 17 cases were analysed by the
Oasys 2 computer program, and three of these had Oasys-2 Scores >2.5.
These cases were felt not to show asthma because PEF d...
We read with interest the paper on glutaraldehyde and symptoms in
endoscopy nursing staff.[1] It is reported that there was an absence of
objective evidence of the physiological changes associated with asthma.
Peak expiratory flow (PEF) records from 17 cases were analysed by the
Oasys 2 computer program, and three of these had Oasys-2 Scores >2.5.
These cases were felt not to show asthma because PEF diurnal variability
was less than 15%. We have recently shown that increased diurnal
variability is not found in the majority of workers with occupational
asthma.[2] Part of the explanation may be that the acrophase (time of
maximum PEF in a 24 hour period) in normal and asthmatic individuals
occurs at around 16:00 hours with a trough about 12 hours later. Any
deterioration in lung function due to exposure in the workplace is
superimposed on the normal circadian rhythm. Thus, if a worker starting
work in the morning has a fall in PEF that continued throughout the day
whilst at work, the maximum PEF occurring at the time of the acrophase
might be reduced. This would tend to reduce the diurnal variability. Even
in non-occupational asthma there is considerable overlap of PEF
variability with that occurring in normal individuals.[3] Use of non-
linear PEF meters significantly underestimates PEF variability [4] but
even when PEF readings are linearised, an absence of an increase in
diurnal variability does not exclude asthma. An Oasys-2 score of >2.5
has a specificity of 94% for diagnosing occupational asthma.[5] We suspect
that, provided peak flow records were of adequate quality, the three cases
with Oasys-2 scores >2.5 did indeed have occupational asthma.
Since 1995, 29 cases of occupational asthma due to glutaraldehyde
have been reported to SHIELD, the West Midlands reporting scheme for
occupational asthma. A study of 24 workers referred to the Occupational
Lung Disease Clinic in Birmingham with respiratory symptoms temporally
related to glutaraldehyde exposure found that 16 had a definite
occupational effect evident on their PEF records.[6] Five of eight workers
with equivocal PEF records underwent specific bronchial provocation tests
to 2% glutaraldehyde, all of which were positive as were three challenge
tests in workers with suggestive PEF records. The challenge subjects
included two in whom PEF diurnal variability was less than 10%. Of the
subjects, 7 out of 24 also had positive specific IgE to glutaraldehyde.
The sensitivity of serial PEF records in showing occupational asthma
drops dramatically if less than three to four weeks of recordings are
performed or if they are of inadequate quality, for example-less than four
readings per day. We have found that objective evidence of glutaraldehyde
induced asthma can be obtained in a large proportion of workers with
respiratory tract symptoms temporally related to glutaraldehyde exposure
when adequately sought after.
W Anees
A S Robertson
P S Burge
Occupational Lung Disease Unit
Birmingham Heartlands Hospital
Birmingham B9 5SS
1. Vyas A, Pickering CAC, Oldham LA, et al. Survey of symptoms,
respiratory function, and immunology and their relation to glutaraldehyde
and other occupational exposures among endoscopy nursing staff. Occup
Environ Med 2000;7:752-9.
2. Anees W, Burge PS. Diurnal variability of peak expiratory flow and non
-specific bronchial reactivity in workers with occupational asthma. Eur
Respir J 2000;16:520s
3. Higgins BG, Britton JR, Chinn S, et al: The distribution of peak
expiratory flow variability in a population sample. Am Rev Respir Dis
1989;140:1368-72.
4. Miles JF, Miller MR: Influence of peak flow meter non-linearity on
recorded PEF variability. Thorax 1992;47:891
5. Burge PS, Pantin CF, Newton DT, et al. Development of an expert system
for the interpretation of serial peak expiratory flow measurements in the
diagnosis of occupational asthma. Occup Environ Med 1999;56:758-64.
6. Di Stefano F, Siriruttanapruk S, McCoach JS, Burge PS. Glutaraldehyde:
an occupational hazard in the hospital setting. Allergy 1999;54:1105-9.
It is good to see some scientific rigour applied in this important
area. It is interesting to note however that there is no definition of
occupational dermatitis. It is a reportable and prescribed disease in the
UK, and can cause major impact on workers who suffer from it, but the
question is whether healthcare workers who have perhaps a period of dry
skin managed with ease, should be regarded has suffering from an
occu...
It is good to see some scientific rigour applied in this important
area. It is interesting to note however that there is no definition of
occupational dermatitis. It is a reportable and prescribed disease in the
UK, and can cause major impact on workers who suffer from it, but the
question is whether healthcare workers who have perhaps a period of dry
skin managed with ease, should be regarded has suffering from an
occupational disease. The answer to such a question is important to the
context of this paper and to the subject as a whole.
The title of the paper is on 'management' therefore relates to those who
have the condition, but there are of course in addition, major issues of
risk reduction and control, which must run in parallel. While the paper
makes mention of sensitisation in its background section, this important
group does not feature in the review.
In its later sections the term occupational dermatitis, is often reduced
just to 'dermatitis'. Does this mean that the recommendations apply
equally to workers with non occupational skin problems, such as psoriasis
or eczema, both in the pre-employment and in service situations?
Recently the results of a comprehensive epidemiological follow up
study of cancer mortality in cohorts with occupational exposure to
acrylamide was published.[1] With the exception of a weak significance for
a raised incidence of pancreas cancer the study arrived by and large at
the conclusion that there is "little evidence for a causal relationship
between exposure to acrylamide and mortality from any c...
Recently the results of a comprehensive epidemiological follow up
study of cancer mortality in cohorts with occupational exposure to
acrylamide was published.[1] With the exception of a weak significance for
a raised incidence of pancreas cancer the study arrived by and large at
the conclusion that there is "little evidence for a causal relationship
between exposure to acrylamide and mortality from any cancer sites". The
study updates and confirms an investigation 10 years earlier of the same
cohorts.[2] The analysis was based on standardised mortality ratios (SMR)
in comparison with US national or relevant county mortality statistics. It
exemplifies the shortcomings of epidemiological studies of this kind to
detect moderate influences of specific causative factors on cancer
mortality or incidence. The investigators praise themselves of having
carried out "the most definitive study of the human carcinogenic potential
of exposure to acrylamide conducted to date". The results, however, pose
questions. Could unacceptable risks be detected? Which risks would have
been expected?
For the US workers the average cumulative exposure is given to 0.25 mg/m3
y. (We assume this to correspond to exposure of the whole factory staff to
0.25 mg/m3 for 365 eight-hour working days). At an alveolar ventilation
rate of 0.2 L/kg min this exposure would mean a cumulative uptake of
about 9 mg acrylamide per kg body weight. This dose corresponds to a
lifetime (70 years) uptake of 0.35 µg/kg d. According to the estimate of
U.S. EPA[3] this would correspond to a cancer risk of 1.6 10-3. An
estimate based on the multiplicative model[4] would arrive at a ca 3 times
higher risk, 5 10-3. With a cancer mortality in the Western World
countries of 0.18, these figures correspond to an 1-3% increase of the
cancer mortality risk, i.e. a RR of 1.01-1.03. Since about one fifth of
the workers were defined as exposed (with greater than or equal to 10-3 mg/m3 years) the relative
risk in the exposed group due to inhalation of acrylamide may have been
about 1.05-1.15.
Although it is doubtful that these risk increments could be considered
negligible, they would not be detectable in a study of the present kind.
Since uptake via the skin often occurs in work leading to inhalation of
acrylamide it is possible that the true risk increments are considerably
higher. If we assume the total relative risk (from inhalation plus dermal
uptake) to be in the range of 1.1-1.2, it is a pertinent question whether
this risk increment is detectable within the large material studied by
Marsh et al.[1]
Like many other materials of similar kinds the data are far from ideal for
epidemiological analyses. The main reasons for this are the skew
distribution of duration of employment, the incompleteness of data for
smoking, and the healthy worker effect. The healthy worker effect leads to
a deficit in death rates from all causes, in the present study by about
20% for all causes except cancers. Deficits in SMR for all malignant
neoplasms and for certain tumour types are also often significant,
although with a disturbing influence of a significantly increased SMR for
lung cancer in an earlier period. (The significant decrease in lung cancer
deaths as well as deaths in diseases of the circulatory system from 1925-
83 to 1984-94 would be compatible with a drastic reduction, before 1984,
of smoking.) It is expected that the healthy worker effect comprises
cancer, at least to some extent, as well as other causes of death.
A straightforward way of overcoming the healthy worker effect is a within cohort analysis of the regression of mortalities or incidences on the
estimated dose. Marsh et al.,[1] have done this for each of a few selected
tumour sites. Due to too few observed deaths in each dose interval the
statistical power of this material is, however, too small to show
anything.
This analysis of individual sites, avoiding a pooling of data that would
increase the statistical power, illustrates the widespread dogma that
different cancer types are affected specifically by carcinogens. It has
been shown for a few mutagenic carcinogens including acrylamide that a
linear multiplicative model, Pj = P0j (1+ ß D), can be fitted to
experimental cancer incidence data and, for radiation, to human data.[5]
Pj and P0j are the total and background risks of tumour at site j, D the
dose and ß a relative risk coefficient that is (at least approximately)
the same for all tumour sites j. ß is thus applicable to pooled data for
groups of sites or for all (responding) sites. Although analysis of death
risks associated with specific tumours has its indisputable value, a
restriction of significance estimation to individual sites leads as a main
effect to a loss of statistical power. For related reasons the
identification of certain sites as "interesting", with reference to
response to acrylamide in animal experiments, is mostly a consequence of
the pattern of background incidences P0j in the animal strain used.
The authors of the paper,[1] possess a material of extreme value in
further efforts to clarify the carcinogenic potency of acrylamide. In view
of the importance of this question we urge the authors of the paper to
continue their work, particularly with analyses of regression on pooled
data, primarily for all cancer, with and without exclusion of smoking related sites.
Fredrik Granath
Dept of Medical Epidemiology,
Karolinka Institute
Lars Ehrenberg
Dept of Genetic and Cellular Toxicology,
Stockholm University
Birgit Paulsson
Margareta Törnqvist
Department of Environmental Chemistry,
Stockholm University,
S-106 91 Stockholm,
Sweden
1. Marsh, GM, Lorraine, JL, Youk AO, Schall LC. Environ Med
1999;56:181-190.
2. Collins JJ, Swaen GMH, Marsh GM, Utidjian HMD, Caporossi JC, Lucas
LJ. J Occup Med 1989;31:614-617.
3. U.S. EPA, United States Environmental Protection Agency.
Assessment of Health Risks from Exposure to Acrylamide. 1990 U.S.
Environmental Protection Agency: Washington, DC.
4. Törnqvist M, Bergmark E, Ehrenberg L, Granath F. [Risk Assessment
of Acrylamide] (in Swedish) National Chemicals Inspectorate, Solna,
Sweden. 1998 PM 7-98.
We thank Dr. Kawada for his interest in our manuscript entitled "Associations of low-level urine cadmium with kidney function in lead workers."[1] As discussed in the methods and shown in the footnotes to Tables 3 and 4 in the manuscript, we adjusted for blood and tibia lead. We have presented lead analyses in this cohort in multiple past publications[2-8] so, in order to focus on the unique cadmium associations and compl...
Dear Editor,
As it had been discussed in the study[1], selection bias may affect the validity of the result. In this case there would be selection bias, if the response rate in the survey associated with occupation, and the distribution of occupation among controls did not reflect that among the general population. However, if the response rate was independent from occupations, health status, other lifestyle, se...
Dear Editor,
This article recalls a controversy of the early 1930s, when the authority of no less a genius than Professor JS Haldane was challenged on behalf of South Wales coalminers by a mining mineralogist W. R. Jones, who as a consequence was to acquire the soubriquet "Sericite". [1]
Their disease was considered by Haldane not to be attributable to the dust to which they were exposed, as its level of c...
Dear Editor,
High temperatures and mortality - even more relevant in desert environments.
Your editorial on exposure to high ambient temperatures and mortality is timely [1]. The Gasparrini et al.[2] paper on ambient air temperatures and mortality in temperate England and Wales provides further support for population-level preventive measures to reduce the likelihood of adverse health effects from elev...
Editor,
I was interested to read the excellent COPE Report Paper[1] and note Occupational and Environmental Medicine's intention to follow these guidelines.
In particular, from the occupational health point of view, I welcome the inclusion of involvement of the study participants in consideration and agreement of the research protocol, though I am a little sad that the COPE Committee...
Editor,
We read with interest a recently published study on personal exposure of asthmatic children to nitrogen dioxide (NO2), relative to concentrations in outdoor air.[1] In their results, authors didn't find: 1. "…significant correlation… between each child's weekly mean personal exposures and mean outdoor concentrations for the corresponding periods"; 2. "…marked evidence of seasonality" on personal exposure...
Cesaroni et al make an assessment of the health benefits of a traffic management scheme in Rome based on changes in vehicle emissions and associated chronic risk factors(1). The authors estimate that a combination of the policy intervention and unrelated fleet changes caused a 38% reduction in the annual mean exposure of NO2 and a 29% reduction of PM10 within the 'railway ring' restricted zone bet...
Editor
We read with interest the paper on glutaraldehyde and symptoms in endoscopy nursing staff.[1] It is reported that there was an absence of objective evidence of the physiological changes associated with asthma. Peak expiratory flow (PEF) records from 17 cases were analysed by the Oasys 2 computer program, and three of these had Oasys-2 Scores >2.5. These cases were felt not to show asthma because PEF d...
It is good to see some scientific rigour applied in this important area. It is interesting to note however that there is no definition of occupational dermatitis. It is a reportable and prescribed disease in the UK, and can cause major impact on workers who suffer from it, but the question is whether healthcare workers who have perhaps a period of dry skin managed with ease, should be regarded has suffering from an occu...
Editor,
Recently the results of a comprehensive epidemiological follow up study of cancer mortality in cohorts with occupational exposure to acrylamide was published.[1] With the exception of a weak significance for a raised incidence of pancreas cancer the study arrived by and large at the conclusion that there is "little evidence for a causal relationship between exposure to acrylamide and mortality from any c...
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