Quoting both dictionary definitions and statuory requirements, Koh
and Aw's education article [1] limits the definition of occupational
"health surveillance" to the detection of adverse health effects resulting
from occupational exposures. In doing so, they exclude international and
national requirements for occupational health and medical surveillance to
assess fitness for work.
Quoting both dictionary definitions and statuory requirements, Koh
and Aw's education article [1] limits the definition of occupational
"health surveillance" to the detection of adverse health effects resulting
from occupational exposures. In doing so, they exclude international and
national requirements for occupational health and medical surveillance to
assess fitness for work.
Looking at the hazard of ionizing radiation, international
recommendations,[2] European Directives [3] and UK National Legislation [4]
all identify a requirement for surveillance where the primary purpose is
an assessment of the individual's fitness for post. Similarly, in
considering surveillance of divers, a key element of requirements is an
assessment of fitness for work. On a more general level, both in the
public and in the occupational setting systems of health surveillance
exist for drivers where it is clearly nonsense to suggest that this is
aimed at the detection of adverse effects resulting from time behind the
wheel. It is therefore suggested that the authors' conclusion needs to be
expanded to identify a requirement for periodic examination of
individuals, not only to detect reversible ill health, but also to assess
fitness for work.
References
(1) Koh D, Aw T-C. Surveillance in occupational health. Occup Environ Med
2003;60:705-710
(2) Recommendations of the International Commission on Radiation Protection
publication 60: 1992
(3) Basic safety standards for the health protection of the general public
and workers against the dangers of ionising radiation European Union
Counsel directive 1996/29/EURATOM 13th May 1996
(4) The Ionising Radiations Regulations 1999 (UK statutory instrument).
Bernard et al.[1] presented results from several studies
investigating childhood asthma in relation to swimming pool use. Though
the studies were generally well-conducted, there are some respects in
which the statistical analysis and interpretation are misleading.
The study of asthma prevalence in relation to swimming pool use was
essentially an ecologic design - the unit of analysis was...
Bernard et al.[1] presented results from several studies
investigating childhood asthma in relation to swimming pool use. Though
the studies were generally well-conducted, there are some respects in
which the statistical analysis and interpretation are misleading.
The study of asthma prevalence in relation to swimming pool use was
essentially an ecologic design - the unit of analysis was the school.
Though the study of correlations between asthma prevalence and indexes of
pool use respects this (the p-values are appropriate), the logistic
regression analysis does not. The analysis is carried out as if there were
1881 independent observations of asthma and swimming pool use. In fact,
observations are not independent - there is “clustering” of asthma by
school - even after allowing for effects of swimming pool use and other
covariates. The extremely low p-values in Figure 6 therefore cannot be
relied on. The analysis applied to the study of chronic effects on lung
epithelium is also limited in not allowing for possible clustering by
school. Again, the p-values presented overestimate the strength of
evidence for an association.
Caution is also required in interpreting the correlations and p-
values in Figures 5C and 5D. These do not test the association of asthma
with pool use, but with a composite index of pool use, pets, and passive
smoking. It is not possible from the results presented to distinguish the
contribution of each. The authors acknowledge this, but reader confusion
may arise because the term "adjusted" is more usually used in epidemiology
to describe adjustment for confounding of one effect by another - this is
not the case here.
Finally, the correlations shown in figures 5A and 5B are selected
from a wider range of measures of pool attendance, as shown in figure 4.
Among these non-independent indices of exposure, the authors have chosen
the one showing the strongest correlation with asthma prevalence. For this
reason, the "significance" of the p-value in figure 5B should be
interpreted as suggestive rather than definitive.
We conclude that the epidemiological evidence for an association of
asthma with swimming pool use is not as strong as claimed by the authors.
Ben Armstrong
Public and Environmental Health Unit
London School of Hygiene and Tropical Medicine
Keppel St
London WC1E 7HT
David Strachan
Department of Public Health Sciences
St. George's Hospital Medical School
Cranmer Terrace
London SW17 0RE
References
(1) Bernard A, Carbonnelle S, Michel O, et al. Lung hyperpermeability
and asthma prevalence in schoolchildren: unexpected associations with the
attendance at indoor chlorinated swimming pools. Occup Environ Med 2003;60:385-94.
I have only recently had an opportunity to see the OEM online abstract of this paper[1] but I did see the unpublished original version in
the Health Department archives whilst I was Chief Medical Officer on
Montserrat from late 1998 to late 2000.
My first comment is that this survey of schoolchildren was carried
out in February 1998 and yet it has only now been published in a
scientific journ...
I have only recently had an opportunity to see the OEM online abstract of this paper[1] but I did see the unpublished original version in
the Health Department archives whilst I was Chief Medical Officer on
Montserrat from late 1998 to late 2000.
My first comment is that this survey of schoolchildren was carried
out in February 1998 and yet it has only now been published in a
scientific journal more than 5 years later. This is of some relevance
since the highlights of the paper published in the BMJ on 12 April 2003 [2] comment that since the time of the first eruption in 1995 the children
“have had an excess of respiratory illness” and that “few were receiving
recommended appropriate treatment”. This statement is misleading. It may
well have been true up until 1998 but it is certainly not true for the
period beyond that time. The reality of children more heavily exposed to
heavy ash falls experiencing more wheeze and asthma than those less
exposed has been convincingly demonstrated in the paper. However most of
the children living on Montserrat since 1998 have been in the north of the
island and only intermittently exposed to relatively lighter falls of ash.
My own clinical experience and that of visiting paediatricians is
that the prevalence of asthma and asthma like symptoms is no higher than
other parts of the Caribbean and may even be lower. A survey carried out
by the Health Department of resident children in June 2000 [3] found the
prevalence of “wheeze ever” in all schoolchildren to be 22.7% (compared
with 27.7% in all children in the 1998 survey). This survey also found the
prevalence of “asthma ever” to be 13.8% compared with 9.8% in the 1998
survey. The 2000 survey found no association with exposure to higher ash
levels but it must be recognised that in 2000 very few children were
exposed to anything like the levels experienced between 1995 and 1998.The
treatment that has been given to children experiencing asthma has been
along conventional lines as recommended by paediatricians in the United
Kingdom.
Further evidence of the lack of any continuing serious adverse
effects of volcanic ash on respiratory health comes from a one year survey
of all clinic attendances by all age groups on Montserrat during 1999..
This survey found no correlation between weekly clinic attendances for
respiratory symptoms and episodes of ash venting or increased ground ash
levels. A further study by the Institute of Occupational Health in
Edinburgh [4] carried out in October 2000 found a prevalence of asthma of
8.1% and of chronic bronchitis of 6.7% in a group of 421 workers on
Montserrat occupationally exposed to high levels of ash. A subsequent
survey of 440 Montserratians relocated to the United Kingdom [5] found a
prevalence of 14.2% for asthma and 14.0% for chronic bronchitis.
My second and most important comment is that by far the most important
adverse effects of the volcanic eruptions relate to the social and
economic disruption and its effect on the life and health of the people.
In my paper in the West Indian Medical Journal [3] I have described a
change in population demographics with a fall in the productive group and
a rise in more dependent people, loss of older female family providers,
more elderly people becoming dependant on the state, increases in anxiety
and depression in the elderly, changes in the diet and increasing obesity
in children and increases in domestic violence.
One of my concerns whilst on Montserrat was that most of the academic
input following the disaster was put into vulcanology and respiratory
health. Some valuable findings have come out of this work but no formal
academic input was made into other more serious matters, especially on the
health side.
Fortunately the outstanding health problems of Montserat have been
addressed by the health department with the help of the UK Department for
International Development and the Pan American Health Organisation but
much remains to be done. The importance of this was dramatically
emphasised with the reports of a massive dome collapse on 12/13th July and
ash venting which uncharacteristically smothered the inhabited north of
the island. Such a big eruption could easily demoralise some of those not
already traumatised. However we can expect the resilience of the remaining
population of around 4500 people to carry them through yet again in spite
of all the social and economic disruption which has had a far more
profound influence on their health than the purely physical effect of the
ash.
References
(1) L Forbes, D Jarvis, J Potts, and P J Baxter. Volcanic ash and respiratory symptoms in children on the island of Montserrat, British West Indies. Occup Environ Med 2003;60:207-211.
(2) BMJ family highlights. Inhaling volcanic ash effects breathing. BMJ2003;326:785.
(3) Avery JG The Aftermath of a Disaster. Recovery Following the Volcanic Eruptions in Montserrat, West Indies. West Indian Medical Journal; in press.
(4) Cowie HA, Searl A, Ritchie PJ, Graham MK, Swales C et al. A health
Survey of Workers on the Island of Montserrat. Research Report.TM/02/02.
Edinburgh: Institute of Occupational Medicine; 2002
(5) Cowie HA, Searl A, Ritchie PJ, Graham MK, Hutchison PA, Pilkington A. A Health Survey of Montserratians Relocated to the United Kingdom.
Research Report TM 01/07. Edinburgh: Institute of Occupational Medicine; 2001.
The hygiene hypothesis has grown into a popular idea for explaining the increase in asthma and atopy in children,[1,2] although it remains
controversial.[3]
This hypothesis can be extended to adults, especially
those in certain occupations. It is suggested that there is another form
of the hygiene hypothesis – called the occupational hygiene hypothesis.[4] In 1965, it was observed that those expos...
The hygiene hypothesis has grown into a popular idea for explaining the increase in asthma and atopy in children,[1,2] although it remains
controversial.[3]
This hypothesis can be extended to adults, especially
those in certain occupations. It is suggested that there is another form
of the hygiene hypothesis – called the occupational hygiene hypothesis.[4] In 1965, it was observed that those exposed to textile (cotton) dust
exhibited a lower than expected rate of lung cancer.[5] This concept was
elucidated in a sentinel paper [6] published in 1985; the authors’
suggested that the agent responsible for reduced lung cancer rates was
endotoxin (lipopolysaccharide), a cell wall component of gram negative
bacteria. Since that time, these initial findings were confirmed by
several epidemiological studies in cotton textile workers, reviewed in a
recent meta-analysis,[7] and by observation in other occupations[8,9]
that are exposed to endotoxin. Finally, an experimental study supported
these epidemiological findings.[10] It is also suggested that such
occurrences exist for other exposures and occupations, but have yet to be
described.[11] This suggests that this is a new area of science that has
not been explored, except by a few.
With the discovery of Toll-like receptors,[12] mechanisms of
endotoxin have been better clarified and explaining how immune stimulation
can result in reduced rates of lung cancer.
Sadly, this letter is dedicated to my mentor (JHL), Professor Jan L.
Sykora, who died on June 25, 2003. He provided me with the wisdom to
explore a murine model [13] for establishing evidence of the “occupational
hygiene hypothesis”.
References
(1) Weiss ST. Eat dirt-the hygiene hypothesis and allergic diseases. N
Engl J Med 2002;347:930-1.
(2) Braback L. Does farming provide protection from asthma and
allergies? Acta Paediatr 2002; 91: 1147-54.
(3) Liu AH, Murphy JR. Hygiene hypothesis: fact or fiction? J Allergy
Clin Immunol 2003; 111: 471-8.
(4) Lange JH, Rylander R, Fedeli U, Mastrangelo G. Extension of the
"hygiene hypothesis" to the association of occupational endotoxin exposure
with lower lung cancer risk. J Allergy Clin Immunol 2003; 112: 219-220
(5) Enterline PE. Mortality among asbestos products workers’ in the
United States. NY Acad Sci 1965; 132: 156-65.
(6) Enterline PE, Sykora JL, Keleti G, Lange JH. Endotoxin, cotton
dust and cancer. Lancet 1985; 2:934-5.
(7) Mastrangelo G, Fedeli U, Fadda E, Milan G, Lange JH. Epidemiologic
evidence of cancer risk in textile industry workers: a review and update.
Tox Ind Health; in press.
(8) Mastrangelo G, Marzia V, Marcer G. 1996. Reduced lung cancer
mortality in diary farmers: is endotoxin exposure the key factor? Am J Ind
Med30:601-609.
(9) Mastrangelo G, Marzia V, Milan G, Fadda E, Fedeli U, Lange JH. 2003a.
An exposure-dependent reduction of lung cancer in dairy farmers. Indoor
and Built Environment;in press.
(10) Lange JH. Anti-cancer properties if inhaled cotton dust: a pilot
experimental investigation. J Environ Sci Health 1992;27A:505-514
(11) Lange JH. Reduced cancer rates in agricultural workers: a benefit
of environmental and occupational endotoxin exposure. Med Hypotheses 2000;
55: 383-5.
(12) Dabbagh K, Lewis DB. Toll-like receptors and T-helper-1/T-helper-
2 responses. Curr Opin Infect Dis 2003;16:199-204
(13) Lange JH, Sykora JL. Evaluation of the anti-cancer properties of aerosolized endotoxin from Enterobacter agglomerans. In The Proceedings 12th Cotton
Dust Research Conference Beltwide Cotton Research Conferencs, New Orleans,
LA January 6-7, 1988, Jacobs RR and Wakelyn PJ, Eds. Memphis: National Cotton
Council, 139-140.
Having suffered from Asthma all my life I am surprised that common
hasards in the daily life of children are not addressed even in the 21st
century. Chlorine in swimming baths was always a problem to me as a
child, it was used far more concentrated than nowadays.
Another very serious trigger was to be found in cardboard containers
of fruit drinks though. I now realise that they contained Sodium...
Having suffered from Asthma all my life I am surprised that common
hasards in the daily life of children are not addressed even in the 21st
century. Chlorine in swimming baths was always a problem to me as a
child, it was used far more concentrated than nowadays.
Another very serious trigger was to be found in cardboard containers
of fruit drinks though. I now realise that they contained Sodium
Metabisulphide as a preserving agent. When the straw was pushed through a
small hole in the carton a high dose of sulphur dioxide was passed into
the stomach with the drink, soon passing into the lungs in concentrations
that caused me great distress. Because of the 'closed loop' nature of the
ingestion, there is no way of the preservative to vent into atmosphere
first.
I believe this packaging and contents are still sold, mainly to
youngsters, who don't understand how damaging it is to the vulnerable.
Parents should be made aware of this danger too.
The paper by Kraus and colleagues[1] in the December 2002 issue of
Occupational and Environmental Medicine addresses the important issue of the
relationship of personal exposure to possible effect in an industrial
setting. After reading this paper I would like to make some comments with
regard to the design, conduct and statistical analysis of the study.
The paper by Kraus and colleagues[1] in the December 2002 issue of
Occupational and Environmental Medicine addresses the important issue of the
relationship of personal exposure to possible effect in an industrial
setting. After reading this paper I would like to make some comments with
regard to the design, conduct and statistical analysis of the study.
In an area where exposure assessment and confounding effects are so
important, it is interesting to see that seemingly important associations
are being drawn with so little information.
Kraus and colleagues state the goal of the paper as “To correlate the
prevalence of respiratory tract symptoms and diseases with dust and fibre
exposure in the soft tissue industry in Germany” rather than to
investigate whether such a relationship actually exists.
The authors state that: “In every company pure cellulose was the
basis of the production process. Recycled paper was not a relevant
component of the products.”, however, in the introduction they site many
references of toxicological studies that used insulation cellulose
(Isofloc, which is ground up used newspapers sprayed with boric acid) and
other not pure cellulose products. The contaminants in used newspapers
with boric acid would be expected to produce a radically different
toxicological response than inhaled pure cellulose. Only studies that
used pure cellulose of similar source and composition as used in the
plants in this study group should be sited and for such studies the route
of exposure and doses should be provided.
Sampling: From the text, it appears that in this study, data was
obtained on dust measurements in various places in the 7 chosen German
soft tissue companies. These were then compared to symptoms of persons
working in these companies.
The authors state that “According to the employers’ information, we
interviewed all persons from the different workshops employed during the
time period 1996–98.” They then explain that “The data concerning dust
measurements were gathered from 1991 to 1997.” Thus, it appears that the
dust measurements were not directly related to the individuals with the
symptoms nor were they even necessarily coinciding with the presence of
the symptoms. There is no mention of how and where within each plant the
exposures were determined, of whether the dust levels were similar from
1991 to 1997 and whether there was any personnel monitoring to determine
exposures. However, the authors do state that “Because of differences in
the exposure intensity between the seven companies a cumulative exposure
index was generated for describing the individual exposure.” And as such
mean exposure levels were used for comparison.
The confidence that can be placed in conclusions drawn from samples
depends in part on sample size. Small samples can be unrepresentative just
by chance, however, the scope for chance errors can be quantified
statistically. Given this importance, why haven’t the authors stated the
sample sizes in each of the groups used in the statistical analyses?
More problematic are the errors that arise from the method by which
the sample is chosen. In situations with high dust levels there is more
likelihood of sampling which would be atypical of the dust levels more
generally. Such systematic errors cannot usually be measured, and
assessment therefore becomes a matter for subjective judgment. Systematic
sampling errors can be avoided by use of a random selection process in
which each working condition has a known (non-zero) probability of being
included in the study sample. However, this requires an enumeration of all
working conditions in each plant over the entire sampling period (1991 –
1998).
Not only was there no mention of such a sampling procedure being
performed in this study but any sensitivity to specific plant conditions
has been lost through the use of mean values.
Group composition: The authors then gloss over the choice of controls
which were persons from the “management department”. Certainly the
working condition and environment of office workers is not comparable to
that of maintenance workers, electricians and mechanics. Also of concern
is the disproportionality in the controls compared to exposed in terms of
number, sex and smoking history. No mention is made of age and how long
the persons in each group worked in the plant. This information would
permit the reader to assess whether the symptoms were associated with
either age or length of employment. Also, the smoking histories are not
comparable between the groups. From the means in Table 1, there is a
positive association between exposure group and smoking which is never
discussed in the paper. If smoking habits were asked “in a detailed way”
as stated, why haven’t the data have been presented? As there appears to
be a dose relationship with smoking and exposure group, the authors should
have discussed in the introduction the possibility that smoking can also
produce similar effects as reported in this paper and provide appropriate
references.
The authors mention using an attenuation factor (“divided by four and
multiplied by individual time of exposure”) under recommendation of
technical experts. This implies that it was not possible to obtain any
kind of relationships using the company individual monitoring data in
relationship to the individuals working in each company. What is the
rational and scientific basis for this? Without such information, the
choice of cut points for the attenuation factor appears arbitrary and
leads the reader to wonder whether the choice of cut points was determined
iteratively in order to find an attenuation factor which produced
correlations?
Statistical analysis: The authors use the Cochran-Armitage trend test
without adjustment for other variables and even say “that the results are
prone to being confounded”. Yet, they discuss at length the results from
this test in Tables 3 and 4. Further, it is not at all clear that even
this analysis was performed correctly. Hothorn and Bretz (2000),[2] explain
that the Cochran-Armitage trend test is a test based upon a linear dose
response relationship and that the test lacks power for other shapes.
Most of the parameters shown in Tables 3 and 4 of the Kraus paper do not
appear to have a linear dose-response.
More details of the results of the logistic regression analyses
should have been presented to support the conclusions stated by the
authors. At least an estimate of the percent variation in the data
explained by each of the logistic regressions should be provided in the
tables in order to assess the importance of each relationship. Grouped
and individual R2 values are well documented in Statistical texts and can
be calculated for each logistic regression in order to assess importance.
Results: The authors should have clearly state whether they used
inhalable dust or respirable dust in each analysis. Respirable is
probably more relevant, however, Table 2 indicates that there were only 24
respirable dust measurements. With 4 exposure categories (Controls,
<_25 _25100="_25100"/>100) and 7 companies this would amount to less than 1
respirable dust sample per category per company over an 8 year of
monitoring period! It is more likely that they used the inhalable dust
measurements for which there were 105 measurements. Even with the
inhalable dust measurements, this would amount to less than one inhalable
dust measurement every two years per category per company!
The authors state that “The mean sampling time was 1.97 hours (range
0.16–3.8).” This amounts to each category in each plant being monitored
for mean of 7.4 hours over a working time of 14,400 hours. Even if all
105 inhalable dust measurements were performed in one work year (which
they were not), each category in each plant would have been monitored for
a mean of 7.4 hours over a working time of approximately 1800 hours/year.
Yet, the authors are suggesting that somehow these few samples are
representative of what 441 workers were exposed to over an 8 year sampling
period. Not only are the samples not chosen correctly but the small
sample size assures that these measurements are not representative.
The need for statistical significance also seems to have escaped the
authors when discussing the disease parameters. The data presented
indicate that none of the disease parameters are significantly different
from the controls, yet the authors state that “However, sinusitis,
laryngitis, and chronic bronchitis (a disease parameter) showed increasing
odds ratios with increasing cumulative dust exposure (table 5).” What is
the validity of stating this when there is no statistical significance in
the relationship?
Again, in the discussion, the authors state that “After adjustment
for smoking habits, chronic bronchitis was no longer significantly
associated with dust or fibre exposure. However, the highest odds ratio
(1.57) in the subgroup with longest and highest exposure suggests some
deleterious potential.“ This is very worrisome that the authors suggest
that there is a ‘deleterious potential’ when in fact there is no
statistical basis from the data (95% CI of 0.7 to 4.0) for making such a
statement.
In Tables 7 and 8 the authors group the ‘Diseases’ as part of the
‘Symptoms’ no longer differentiating between Diseases and Symptoms.
They then go on to state that “For example, intensity and duration of
exposure have an almost equal influence on the symptom “blocked nose”. The
calculated ORs rise with increasing exposure intensity from 6.4 to 10.8
and with increasing exposure duration from 6.4 to 12.5.” Fortunately,
in Table 7 they present the 95% confidence limits which are (shown in
parenthesis) for these values 6.4 (1.2 to 49.7) and 10.8 (2.9 to 70.5)
which suggest that 6.4 is not different from 10.8 statistically. Not
surprising given the statements by Kraus and colleagues, Tables 7 and 8
present no measure of statistical significance for any of the parameters
yet they state that “For symptoms of the upper airways, clear dose-
response relations could be found with relation to cumulative exposure
indices”. This is certainly not supported by the data presented in these
tables.
Discussion: Again the authors cite references to articles not
dealing with the same pure cellulose as used in the plants. If there are
studies using the same pure cellulose, then a discussion of the route of
exposure and the exposed dose compared to what is seen here should have
been included.
The Ericsson reference and others are not quoted correctly from the
publications. As an example, Ericsson states that “There was a dose-
dependent increase of symptoms from the upper respiratory tract. However,
coughing and coughing with phlegm were not found to be more common among
persons with heavy exposure compared to those with low exposure to the
dust“, indicating that the Ericsson results are not comparable to those in
the current manuscript.
The statement by the authors that “As expected, because of the
distribution of inhalable and respirable dust fraction, symptoms of the
lower respiratory tract have a weaker association with exposure after
adjustment for confounders (for example, cough, phlegm, dyspnoea, and
exercise induced dyspnoea)” should from the data presented in the paper be
changed to state that “As expected, due to the distribution of inhalable
and respirable dust fraction, symptoms of the lower respiratory tract have
no statistically significant association with exposure after adjustment
for confounders (e.g. cough, phlegm, dyspnea, exercise induced dyspnea).”
The question of respirator use in the plants should have been
investigated. If respirators were used even by some employees, then any
association to the measured dust levels for those persons is no longer
valid.
I hope that the critical readers of your journal will decide based
upon the statistical significance of the data whether there is a basis for
stating that a relationship exists between exposure and effect in the soft
tissue industry.
References
(1) T Kraus, A Pfahlberg, O Gefeller, H J Raithel, Respiratory
symptoms and diseases among workers in the soft tissue producing industry. Occup Environ Med 2002;59:830–835.
(2) Hothorn LA and Bretz F. Evaluation of Animal Carcinogenicity
Studies: Cochran-Armitage Trend Test vs. Multiple Contrast Tests.
Biometrics Journal 2000;42(5):553-567.
The aetiology of Parkinson's disease (PD) remains unknown, despite the elapse of more than 185 years since the description of the disease by James Parkinson in 1817.[1]
Niehaus and Lange[2] suggested that environmental endotoxin, lipopolysaccaride produced by salmonella minnesota, might be a risk factor for PD. The authors' conclusions were based on experimental studies and few case reports.
The aetiology of Parkinson's disease (PD) remains unknown, despite the elapse of more than 185 years since the description of the disease by James Parkinson in 1817.[1]
Niehaus and Lange[2] suggested that environmental endotoxin, lipopolysaccaride produced by salmonella minnesota, might be a risk factor for PD. The authors' conclusions were based on experimental studies and few case reports.
I think that environmental toxins in general could explain few cases of PD or even special forms as the postencephalitic one. However, the aetiology of the classical idiopathic PD, which represents the majority of cases, is not clear till now.
Epidemiological studies that evaluated the association between environmental toxins and the risk of PD have reported inconsistent results. Rural residence, drinking well water, and exposure to pesticides did not show conclusive findings (table 1).[3]
Table 1 The association between environmental toxins and Parkinson's disease in selected case-control studies.
Authors
Publication
Year
Rural
residence
Drinking
Well Water
Exposure to
Pesticides
Preux et al.
2000
1.67 (1.00 -
2.50)
1.21 (0.77 –
1.91)
1.34 (0.83 -
2.15)
Taylor et al.
1999
1,07 (0,99
-1,15)
0,93 (0,88 –
0,98)
1,02 (0,90 -
1,17)
Kuopio et al.
1999
1,45 (0,88 -
2,41)
1,48 (0,44 –
4,95)
1,02 (0,63 -
1,65)
Werneck and Alvarenga
1999
1,00 (0,52 -
1,95)
1,49 (0,74 –
3,01)
2,49 (0,53 -
13,14)
McCann et al.
1999
1,70 (1,17 -
2,57)
0,60 (0,38 –
0,92)
1.20 (0,80 -
1,50)
Chan et al.
1998
0,92 (0,59 -
1,43)
1,04 (0,70 –
1,54)
0,75 (0,26 -
2,22)
Liou et al.
1998
2,04 (1,23 -
3,38)
1,07 (0,19 –
5,98)
2,89 (2,28 -
3,66)
Seidler et al.
1996
1,00 (0,70 -
1,40)
0,80 (0,60 –
1,20)
1,60 (1,10 -
2,40)
Morano et al.
1994
2.50 (1.36 -
4.61)
2.77 (1.45 –
5.33)
1.73 (0.95 -
3.15)
Semchuk et al.
1993
0,80 (0,50 -
1,20)
1,10 (0,60 –
2,00)
2,30 (1,30 -
4,00)
Ho et al.
1989
4,90 (1,40 -
18,2)
---
3,60 (1,00 -
12,9)
* Odds ratio with its 95% confidence interval
between parentheses.
In addition, in many of these studies, criteria of diagnosis were not established and diagnosis was not confirmed by neurologist, rising high suspicion towards their results and conclusions.
We should also remember that at the time of data collection and examination of the cases, the premorbid epoch is normally remote in time, and the second alarming question will be: Is it likely that recall of relevant information is inadequate because of the effects of age and, possibly, of the disease its self?
Ward and his colleagues [4] after their twin study stated that the major factors in the aetiology of PD are nongenetic, however it is believed that multiple interactions occur in PD, resulting in a complex trait, which includes genetic, acquired and environmental components. Importance of the gene-environment interplay should be emphasized in most chronic multifactorial diseases occurring in the adult life as PD. Based on that issue, Langston [1] proposed that clinical manifestation in PD is a threshold phenomenon that occurs when neural loss can no longer compensate for normal functioning, and mentioned process is influenced not only by inherited predisposition but by an overall effect of life-long exposures to various environmental factors.
Aetiology of idiopathic PD is still a question for scientists, and calls for further research, especially with the growing proportion of elderly and rising incidence of PD worldwide.
References
(1) Langston JW. Epidemiology versus genetics in Parkinson's disease: progress in resolving an age-old debate. Ann Neurol 1998;44(suppl 1):S45-S52.
(2) Niehaus I, Lange JH. Endotoxins: is it an environmental factor in the cause of Parkinson's disease? Occup Environ Med 2003;60:378.
In a recent article of Occupational and Environmental Medicine [1],
Mannetje and co-workers presented quantitative evidence of an exposure-
response relationship between occupational exposure to crystalline silica
and silicosis mortality in a carefully designed pooled analysis. This
paper impressively demonstrated that simple silicosis, one of the oldest
occupational diseases, is still a relevant occup...
In a recent article of Occupational and Environmental Medicine [1],
Mannetje and co-workers presented quantitative evidence of an exposure-
response relationship between occupational exposure to crystalline silica
and silicosis mortality in a carefully designed pooled analysis. This
paper impressively demonstrated that simple silicosis, one of the oldest
occupational diseases, is still a relevant occupational health problem
nowadays which may have a negative effect on the longevity of silica
exposed workers. The quantitative evidence (exposure-response
relationship) presented in this paper provided a sophisticated basis for
quantitative assessment of the risks of silicosis deaths for workers
exposed to different level of crystalline silica.
In this manuscript, the authors exemplarily quantified the risk of
silicosis deaths for workers exposed to crystalline silica at exposure
levels of 0.1 and 0.05 mg/m³ for 45 years. The estimated lifetime risks of
silicosis death were 13 and 6 per 1000, respectively. The authors
concluded that, due to exposure misclassification and possible under-
report of silicosis deaths, the lifetime risks of silicosis deaths may be
underestimated. However, some methodological limitations related to this
estimation may, on the other hand, lead to an extreme overestimation of
these lifetime risks. One important limitation may be the lack of
consideration of latency period in the assessment. The authors reported in
their paper that workers who died of silicosis had a median duration of
exposure of 28 years and only 9% of silicosis death occurred within one
year after leaving the job. The median latency of silicosis death may,
therefore, account for at least 28 years. If we consider this latency
period (28 years) in a quantitative risk assessment of silicosis deaths
for German workers (life table of German population is used in the
assessment) exposed to crystalline silica at exposure levels of 0.1 and
0.05 mg/m³ for 45 years, we get a lifetime risk of silicosis death of 1.6
and 0.7 per 1000, respectively. These values are about 9 times lower than
the estimates given by Mannetje et al. Even though, we believe that these
values are more likely be overestimated, since the assumption of a 28-year
latency is the most conservative assumption. Furthermore, this latency was
estimated form workers exposed to a much higher level of Quartz (median
cumulative exposure of 7.15 mg/m³-year) than the maximal possible exposure
level in the quantitative risk assessment (maximal cumulative exposure of
4.5 mg/m³-year). Therefore, longer latency period should be considered in
a more realistic assessment. If latency period is not considered in our
assessment, we will get nearly the same results as those given by Mannetje
et al. (see Table 1).
Reference
(1) Mannetje A, Steenland K, Attfield M, et al. Exposure-response analysis
and risk assessment for silica and silicosis mortality in a pooled
analysis of six cohorts. Occup Environ Med 2002; 59: 723-728.
Table 1. Estimated lifetime risk of silicosis death for German
workers exposed to crystalline silica for 45 years
Exposure level
Estimated lifetime risk* (per 1000)
Latency not considered
Latency considered for 28 years
0.05 mg/m³
5.3
0.7
0.1 mg/m³
11.4
1.6
*Life table of German population in the year of 1995 was used in the
assessment
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.
Dear Editor
Quoting both dictionary definitions and statuory requirements, Koh and Aw's education article [1] limits the definition of occupational "health surveillance" to the detection of adverse health effects resulting from occupational exposures. In doing so, they exclude international and national requirements for occupational health and medical surveillance to assess fitness for work.
Looking at th...
Dear Editor
Bernard et al.[1] presented results from several studies investigating childhood asthma in relation to swimming pool use. Though the studies were generally well-conducted, there are some respects in which the statistical analysis and interpretation are misleading.
The study of asthma prevalence in relation to swimming pool use was essentially an ecologic design - the unit of analysis was...
Dear Editor
I have only recently had an opportunity to see the OEM online abstract of this paper[1] but I did see the unpublished original version in the Health Department archives whilst I was Chief Medical Officer on Montserrat from late 1998 to late 2000.
My first comment is that this survey of schoolchildren was carried out in February 1998 and yet it has only now been published in a scientific journ...
Dear Editor
The hygiene hypothesis has grown into a popular idea for explaining the increase in asthma and atopy in children,[1,2] although it remains controversial.[3]
This hypothesis can be extended to adults, especially those in certain occupations. It is suggested that there is another form of the hygiene hypothesis – called the occupational hygiene hypothesis.[4] In 1965, it was observed that those expos...
Dear Editor
Having suffered from Asthma all my life I am surprised that common hasards in the daily life of children are not addressed even in the 21st century. Chlorine in swimming baths was always a problem to me as a child, it was used far more concentrated than nowadays.
Another very serious trigger was to be found in cardboard containers of fruit drinks though. I now realise that they contained Sodium...
Dear Editor
The paper by Kraus and colleagues[1] in the December 2002 issue of Occupational and Environmental Medicine addresses the important issue of the relationship of personal exposure to possible effect in an industrial setting. After reading this paper I would like to make some comments with regard to the design, conduct and statistical analysis of the study.
In an area where exposure assessment...
Dear Editor
The aetiology of Parkinson's disease (PD) remains unknown, despite the elapse of more than 185 years since the description of the disease by James Parkinson in 1817.[1] Niehaus and Lange[2] suggested that environmental endotoxin, lipopolysaccaride produced by salmonella minnesota, might be a risk factor for PD. The authors' conclusions were based on experimental studies and few case reports.
I thin...
Dear Editor
In a recent article of Occupational and Environmental Medicine [1], Mannetje and co-workers presented quantitative evidence of an exposure- response relationship between occupational exposure to crystalline silica and silicosis mortality in a carefully designed pooled analysis. This paper impressively demonstrated that simple silicosis, one of the oldest occupational diseases, is still a relevant occup...
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...
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