Environmental Health - Latest Comments

Authors' Response by Lisa G. Gallagher, Veronica M. Vieira, David M. Ozonoff, Thomas F. Webster and Ann Aschengrau

Ann Aschengrau — 2011-11-10T14:28:01Z

Dr. Bukowski, writing at the request of the Halogenated Solvents Industry Association (HSIA), calls into question our results on the grounds that they conflict with occupational studies he alleges show no increased risk of breast cancer at much higher PCE exposures. We understand why the HSIA would want to weigh in on this question because it might suggest that their product, PCE, which is in widespread use and causes extensive exposure in the occupational and general community environment, is an unreasonably dangerous product. Given the size of the exposed population, even relatively small risks could result in an unacceptable breast cancer burden on society.

The majority of the occupational studies he cites examined breast cancer mortality, not incidence, as the outcome, and, as such, did not assess associations with the entire spectrum of this, often non-fatal, disease. These studies also had little adjustment for confounding factors and are confounded by socioeconomic status (SES), an important risk factor for breast cancer. This source of confounding would tend to bias the results of the occupational studies towards the null because low SES women tend to be employed in PCE-exposed occupations while high SES women have an increased risk of breast cancer. In contrast, our study considered and controlled for many potential confounding variables, including a woman's educational level. In our general population study subjects we found little evidence of confounding by SES because the irregular pattern of PCE contamination on Cape Cod often resulted in vastly different exposure levels for adjacent residents and neighborhoods. In addition, the different exposure routes in the occupational studies (e.g. mainly inhalation and dermal) may contribute to the alleged divergent findings between our study and this body of literature.

There are also several statements made by Dr. Bukowski that are incorrect. First, the author misinterpreted our exposure measure as an actual mass value in grams. As noted in our paper, our cumulative measure of PCE exposure was not a mass (a ratio measure), but an ordinal measure used to rank our subjects. In addition, the author's statement that our study results are not internally consistent inaccurately represents our data by mixing results for any exposure with those for exposure levels. Our paper noted no increases in the crude odds ratios until 17 and 19 years latency (ORs 1.3-1.4) among ever-exposed women and stated that adjusted odds ratios among ever-exposed women were null for all latent periods.

Each latency analysis also used a latency-specific exposure distribution to determine percentile cut points. Thus, varying results across latent periods may reflect different cut points (paper Table 2). The cut point for current smoothing analysis (RDD>35) is most comparable to the 90th percentile cut point used in the prior analysis. In addition, some odds ratios for the current 90th percentile may be attenuated because of the lower cut points. In general, the reduction of exposure misclassification resulted in assigning subjects who were unexposed in the prior analysis to low exposure in the current analysis. This change resulted in a cleaner referent population and was expected to strengthen the associations. However, the low exposures determined by the automated method were associated with little or no increased risk.

In summary, we maintain that the new exposure assessment method described in this paper is improved from the original method, as evidenced by an improved correlation with sampling data and reflecting a more accurate estimate of water flow in the piping network. An important contribution of this analysis was to demonstrate that the associations between breast cancer and PCE-contaminated drinking water are relatively robust to refinements in exposure modeling.

Comment on the paper by Gallagher et al.: Risk of breast cancer following exposure to tetrachloroethylene-contaminated drinking water in Cape Cod, Massachusetts: reanalysis of a case-control study using a modified exposure assessment.

John Bukowski — 2011-10-19T16:31:32Z

In this most recent iteration of the Cape Cod perchloroethylene (PCE) study, Gallagher et al. [1] have attempted to improve the exposure assessment used in the previous breast cancer articles [2,3]. However, these authors are still left with the same problem, trying to tease out relatively weak effects from residential exposure, when much higher occupational and laboratory exposures have failed to demonstrate them.

The results reported by Gallagher et al. are in conflict with those of occupational studies in which women were exposed to much higher levels. Assuming that the relative delivered dose (RDD) from the current paper is in grams, women on Cape Cod experienced median cumulative (ie, total) exposures of approximately 2 grams PCE [1]. Using calculations from my recent review on the epidemiology surrounding residential PCE, average occupational exposure from dry cleaning in the 1970s (which is germane to the occupational studies published in the literature) is estimated at 100-700 mg per day [4]. Assuming a 200-day work-year, dry cleaning had exposed working women to 20-140 grams PCE per year, or 400-2800 grams during a 20-year working life. Yet, Gallaher et al. acknowledge that ¿in general, null effects have been found for breast cancer¿ in this literature. In their discussion, these authors cite several isolated studies as support for an epidemiologic link between PCE and breast cancer [1]. Yet, neither authoritative reviews [5-9] nor large cohort studies [10,11] have concluded that there is any relationship, despite the aforementioned several orders of magnitude greater exposure for dry cleaners compared with women in Cape Cod. Gallagher et al. also acknowledge that laboratory studies fail to show a relationship between high-level PCE exposure and mammary cancer [1].

The results of the current study are also internally inconsistent. Gallagher et al. state that there was ¿no increase in the odds ratio until 17 and 19 years of latency.¿ But, their adjusted ORs of 1.3-1.4 for the lower latency categories are essentially the same as for those with 11 or more latent years (OR 1.3-1.5), especially given the statistical variability suggested by the confidence intervals [1]. Such findings are inconsistent with the known latency for breast cancer, in which a median latency as long as 22 years has been proposed [12]. Furthermore, none of the ORs reported by Gallagher et al. are statistically significant [1].

Gallagher et al. similarly provide no evidence of any monotonic exposure-response trend that would support a causal relationship. There is no increased risk for ever vs. never exposure, and the risks for those above either the median or 75th percentile are essentially the same as for those below the median (0.9-1.2), especially when statistical variability is considered [1]. This lack of trend would be even more pronounced if exposure groups were appropriately defined as discrete categories of increasing exposure such as quartiles or deciles. Instead, Gallagher et al. provide exposure categories nested within those below them. That is to say, those above 50% include those above 75%, which in turn include those above 90%. This sliding scale hides irregularities in exposure-response that would further detract from causal confidence. For example, adjusted ORs for those in the highest decile are 1.3-1.5, compared with 0.9-1.1 for those above the 50th or 75th percentiles. The high-risk women above the 90th percentile are included within these lower categories, so the risks from lower exposure would be greatly reduced if those with highest exposure were removed. For this reason, more appropriate categories such as 50%-75% and 75%-90% would most likely have shown OR below 1.0 (ie, protective), which is highly inconsistent with any positive trend from increasing exposure.

Gallagher et al. suggest that they have enhanced the previous Cape Cod breast cancer methodology by refining the exposure metric to reduce misclassification [1]. Although the original misclassification purportedly had a greater impact on those with lower exposure, it was still ostensibly nondifferential, meaning similarly distributed among cases and controls. Such misclassification should bias toward the null, so that improved estimates tend to elevate risks. Yet, in the current situation, most revised OR have been driven downward, including those among the highest exposure decile who were least impacted by the misclassification. Most noteworthy are risks among those with exposure below the median, for whom OR of 1.2-2.1 (from the earlier study iterations) have been completely eliminated by ostensibly decreasing nondifferential exposure misclassification (see table 5, ref. [1]). Given that such findings go against expectation, one cannot help but wonder if some degree of ¿data shopping¿ has been carried out in order to explain away these previous contrary findings.

Gallagher et al. acknowledge that there may have been residual confounding, but discount that as an explanation for results given that ¿the irregular pattern of the ACVL pipe locations¿ would make a differential association with exposure unlikely [1]. Yet, the core confounders must have been differentially distributed by exposure, because adjustment for them decreased OR by as much as 50% (see table 4, ref. [1]). Although not yet proven risk factors, other potential confounders such as bone density, use of estrogen replacement therapy, alcohol intake, diet, and obesity have relative risks similar to those associated with some of the core confounders adjusted for in the current study [13-15]. A model-building process with adjustment for a suite of these other factors (rather than one at a time) may have lowered ORs even further. Also, given that confounding covariates (like exposures) are measured imprecisely, residual confounding from risk-factor misclassification is possible even after adjustment [16, 17]. Therefore, residual confounding should be considered as at least a partial explanation for the reported results.

In conclusion, Gallagher et al. have shown different results using the EPA automated model, but have not proven that this is a superior method to the previous manual method. There was a slightly better correlation between measured and modeled values using the automated method (r=0.65) compared with the manual one (r=0.54). But as the authors point out, the measured values ¿are not a standard at all but just another view of the data¿ [1]. Therefore, given the lack of any gold standard by which to judge that the different results produced by Gallagher et al. are superior (ie, closer to the truth) to those produced previously, the current paper appears to be an academic exercise that adds little useful information to the literature on breast cancer causation. Furthermore, the information that it does provide fails at least four of Hill¿s criteria for causation. Namely, the association is weak, inconsistent with the existing human and experimental evidence, and lacking an exposure-response trend [18]. Given these limitations, the results warrant cautious interpretation and do not support a causal relationship between breast cancer and PCE exposure.

References
1. Gallagher LG, Vieiria VM, Ozonoff D, Webster TF, Aschengrau A: Risk of breast cancer following exposure to tetrachloroethylene-contaminated drinking water in Cape Cod, Massachusetts: reanalysis of a case-control study using a modified exposure assessment. Environ Health 2011, 10:47 Available from: http://www.ehjournal.net/content/10/1/47.

2. Aschengrau A, Paulu C, Ozonoff D: Tetrachloroethylenecontaminated drinking water and the risk of breast cancer. Environ Health Perspect 1998, 106 (Suppl 4):947¿953.

3. Aschengrau A, Rogers S, Ozonoff D: Perchloroethylenecontaminated drinking water and the risk of breast cancer: additional results from Cape Cod, Massachusetts, USA. Environ Health Perspect 2003, 111:167¿173.

4. Bukowsk JA: Review of the epidemiologic literature on residential exposure
to perchloroethylene. Crit Rev Toxicol 2011: 1¿12. Available early online from: http://informahealthcare.com/doi/abs/10.3109/10408444.2011.581649.

5. Weiss NS: Cancer in relation to occupational exposure to perchloroethylene. Cancer Causes Control 1995, 6:257-266

6. Lynge E, Anttila A, Hemminki K: Organic solvents and cancer. Cancer Causes Control 1997, 8:406-419

7. Institutes of Medicine: Gulf war and health. Vol. 2: Insecticides and solvents. Washington, DC: National Academies Press; 2002.

8. Mundt KA, Birk T, Burch MT: Critical review of the epidemiological literature on occupational exposure to perchloroethylene and cancer. Int Arch Occup Environ Health 2003, 76:473-491.

9. Ruder AM: Potential health effects of occupational chlorinated solvent exposure. Ann NY Acad Sci 2006, 1076: 207¿227.

10. Boice JD, Marano DE, Fryzek JP, Sadler CJ, McGlaughlin JK: Mortality among aircraft manufacturing workers. Occup Environ Med 1999, 56:581-597.

11. Blair A, Petralia SA, Stewart PA: Extended mortality follow-up of a cohort of dry cleaners. Ann Epidemiol 2003, 13:50-56.

12. Olsson H, Baldetorp B, Ferno M, Perfekt R: Relation between the rate of tumour cell proliferation and latency time in radiation associated breast cancer. BMC Cancer 2003, 3:11. Available from: http://www.biomedcentral.com/1471-2407/3/11.

13. McPherson K, Steel CM, Dixon JM: Breast cancer-epidemiology, risk factors, and genetics. BMJ 2000, 321:624-628.

14. McTiernan A: Behavioral risk factors in breast cancer: Can risk be modified? Oncologist 2003, 8:326-334.

15. Santen RJ, Boyd NF, Chlebowski RT, Cummings S, Cuzick J, Dowsett M, Easton D, Forbes JF, Key T, Hankinson SE, Howell A, Ingle J: Critical assessment of new risk factors for breast cancer: considerations for development of an improved risk prediction model. Endocrine-Related Cancer 2007, 14:169-187.

16. Greenland S: The effect of misclassification in the presence of covariates. Am J Epidemiol 1980, 112:564-569.

17. Marshall JR, Hastrup JL: Mismeasurement and the resonance of strong confounders: Uncorrelated errors. Am J Epidemiol 1996, 143:1069-1078.

18. Hill AB: The environment and disease: association or causation? Proc R Soc Med 1965, 58:295-300.

Estimation of dispersion parameter sigma

Christian Schindler — 2011-03-18T15:02:36Z

In section 5.4, describing the estimation of the dispersion parameter sigma_d it should be written "until a maximum of the likelihood function is reached".

Comment on the paper by Dufault et al.: Mercury in foods containing high-fructose corn syrup in Canada

Karen Rideout — 2010-07-21T12:56:08Z

In January 2009, contemporaneously with the Dufault et al. paper in Environmental Health [1], the Institute for Agriculture and Trade Policy (IATP), a non-profit organization focusing on food, agriculture, and trade, released a report of its own examining the mercury content of foods (such as sodas, syrups, and jams) containing high-fructose corn syrup (HFCS). Dufault et al. [1] tested 20 samples of HFCS from three manufacturers. Nine had detectable levels of mercury (≥0.005 µg/g), ranging from 12,000 to 570,000 ppt (0.012 to 0.570 µg/g) HFCS. Based on these results, the average daily exposure to mercury from HFCS could be 0 to 28.4 µg, about the same as that from dental amalgam [1]. This level of intake is potentially above the provisional tolerable weekly intake (PTWI) for inorganic mercury (i.e., all foods other than fish or shellfish) of 4 µg/kg body weight recently set by the Joint FAO/WHO Expert Committee on Food Additives [2], particularly for children. (The PTWI corresponds to a maximum daily intake of 0.57 µg/kg/day). The ITAP tested 55 foods with HFCS as the first or second ingredient. Mercury was detected in 17 samples, with an average of 128 ppt (range ND–350 ppt) [3]. Both Dufault et al. and the ITAP attributed the finding of mercury to contamination of HFCS through the use of mercury-grade caustic soda (i.e., produced using a mercury cell process, versus diaphragm or membrane cell technology) in its fabrication [1, 3]. Glucose-fructose is produced in Canada and the US, as well as globally, from domestic and imported ingredients. However, it is difficult to ascertain the source of HFCS or raw materials such as caustic soda used in any given food product.

These results prompted us to explore the potential risk of mercury exposure to Canadians through HFCS (referred to as glucose-fructose on Canadian food labels). Because bulk samples of glucose-fructose were not available, we selected nine Canadian national brand retail syrup products with glucose-fructose listed as the first or second ingredient. Although we did not exhaustively sample products from across the country, we tested all national brands of table syrup available at every major chain grocery store in Vancouver. We expect this to be a reasonable representation of retail products available anywhere in Canada. We limited our testing to syrup products as these contain fewer additional ingredients than other more complex food products; they also provided a consistent matrix for laboratory testing.

Total mercury levels were measured at the Trace Metals division of the Complex Biochemistry Laboratory at British Columbia Children’s Hospital. Analysis was done using inductively coupled plasma mass spectrometry (ICP-MS) on a Perkin Elmer Elan 6100 DRC, which is the standard method for trace metal analysis on biological samples. Samples were run in duplicate, spikes were used to measure recovery, and distilled water blanks were run between each sample to prevent cross contamination.

Mercury concentrations ranged from 220 to 1920 ppt (0.220–1.92 µg/l). These results were much lower than the raw HFCS data from Dufault et al., and approximately a factor of ten times higher than the foods sampled by IATP. This does not seem inconsistent, given that Dufault et al. tested raw HFCS and IATP sampled a variety of food products, while we sampled syrup products exclusively. However, all the foods sampled by both IATP and BCCDC contained HFCS (glucose-fructose) as the first or second ingredient. Although one might assume that syrup products would contain more HFCS than general grocery items, the actual percentage of HFCS by weight or volume is not known for any of the foods. Direct comparisons between any of the data are not possible because each investigator tested different products (pure HFCS samples were not available to IATP or BCCDC).

The average mercury concentrations in the products we tested are listed below:
– “Brand A” Golden Corn Syrup – 0.22 µg/l
– “Brand B” Pancake Syrup – 0.25 µg/l
– “Brand B” Original Pancake Syrup – 0.45 µg/l
– “Brand C” Concord Grape Spread – 0.49 µg/l
– “Brand D” Original Syrup – 0.52 µg/l
– “Brand E” Syrup – 0.60 µg/l
– “Brand F” Golden Corn Syrup – 0.84 µg/l
– “Brand G” Corn Syrup – 0.90 µg/l
– “Brand F” Original Syrup – 0.92 µg/l
– “Brand H” Organic Light Corn Syrup – 1.07 µg/l
– “Brand I” Original Syrup – 1.09 µg/l
– “Brand J” Original Syrup – 1.92 µg/l
Although the manufacturer’s website for the organic product (Brand H) states that it is not high-fructose corn syrup, we included it as a possible control, otherwise similar to those containing glucose-fructose.

We calculated several scenarios of mercury intake from glucose-fructose syrups based a diet consisting of 10%, 20%, or 50% of energy intake from retail table syrup. Given the prevalence of glucose-fructose as a sweetener in packaged foods, it is plausible to assume that some individuals might consume 50% of their energy as glucose-fructose. With a mercury concentration of 1.92 µg/l, daily consumption of 300 ml syrup — corresponding to approximately 50% of energy intake — would provide a mercury intake of 0.576 µg/day, i.e., 0.00823 µg/kg/day for a 70 kg man.

None of the mercury in these samples was characterized. Assuming the source of any mercury contamination in HFCS is mercury grade caustic soda, it is likely that it is in the inorganic (rather than more toxic methylated) form. The World Health Organization (WHO) estimates that average daily inorganic mercury exposure from food is 4.2 µg (0.6 µg from fish and 3.6 µg from non-fish sources [4], which is a factor of ten higher than our worst case scenario estimate based on BCCDC data. As well, our scenario is a factor of 1000 times below the JECFA PTWI for inorganic mercury. Even if the mercury in HFCS were methylated during processing, levels are well below Health Canada guidelines. (The maximum provisional tolerable daily intake of methyl mercury for pregnant women, women of childbearing age and young children is 0.2 µg/kg/day) [5].

Despite low levels and questions regarding chemical speciation, detection of mercury in HFCS should not be ignored as a contribution to total mercury exposure. Moreover, unlike fish, for which consumption is recommended despite methyl mercury contamination, HFCS provides no health benefits. Given that alternatives to mercury grade caustic soda are available and mercury cell technology presents environmental and occupational health risks, it would be prudent to avoid its use in food production.

Sincerely,

Karen Rideout¹, Vanita Sahni², Ray Copes³, Mark Wylie⁴, and Tom Kosatsky^1,2

¹ National Collaborating Centre for Environmental Health
² Environmental Health Division, British Columbia Centre for Disease Control
³ School of Population and Public Health, University of British Columbia
⁴ Complex Biochemistry Laboratory, BC Children’s Hospital

References
1. Dufault, R., et al., Mercury from chlor-alkali plants: measured concentrations in food product sugar. Environmental Health, 2009. 8(1).
2. JECFA, Joint FAO/WHO Expert Committee on Food Additives, Seventy-second meeting, Summary and Conclusions. 2010, Food and Agriculture Organization of the United: Rome. [cited 2010 July 20]; Nations & World Health Organization Available from: http://www.who.int/foodsafety/chem/summary72_rev.pdf.
3. Wallinga, D., J. Sorensen, Mottl, P., and B. Yablon, Not so sweet: missing mercury and high fructose corn syrup. 2009, Institute for Agriculture and Trade Policy: Minneapolis, MN. [cited 2009 April 30]; Available from: http://www.iatp.org/iatp/publications.cfm?accountID=421&refID=105026.
4. WHO, Elemental Mercury and Inorganic Mercury Compounds: Human Health Aspects. 2003, World Health Organization: Geneva. [cited 2010 April 13]; Available from: http://www.who.int/ipcs/publications/cicad/en/cicad50.pdf.
5. Health Canada. Mercury: Your Health and the Environment. 2004 December 14, 2007 [cited 2010 April 13]; Available from: http://www.hc-sc.gc.ca/ewh-semt/pubs/contaminants/mercur/index-eng.php.

Authors' response

Conor Reynolds — 2010-02-09T13:29:36Z

It could be said that a gauge of an issue's importance is the passion it inspires, and the safety of cyclists is certainly an issue that people are passionate about. However, passions can be obstacles to collegial discourse. Our review was an attempt to conduct an objective review of the scientific, evidence-based literature on the influence of infrastructure on cycling safety. An important function of a review paper is to compile the relevant literature, so that everyone can use the list to locate and examine original sources. Readers can then evaluate the conclusions of the review paper, based on their own interpretation of the empirical evidence. We trust that interested readers will do just that, as Forester has done.

We have done our best to ensure that this literature review is as complete as possible, within the scope that we have outlined. We restricted ourselves to the peer-reviewed English language literature. The commenter mentions that we missed "the Copenhagen studies". This comment refers to a report [1] that in fact illustrates some of the difficulties with including non-peer-reviewed literature. The methods and results are not described sufficiently for us to be able to abstract and interpret the data. It would be a wonderful contribution for this research to be completely described in the peer-reviewed literature in the future. When and if any additional literature is considered, it will be important to put it in the context of the weight of evidence from existing studies, as we have attempted to do in our review.

C. Reynolds, M. Harris, K. Teschke, P. Cripton and M. Winters

Reference

1. Jensen, SU, Rosenkilde, C, Jensen, N: Road safety and perceived risk of cycle facilities in Copenhagen. Copenhagen, Denmark: Trafitec, Inc. [English-language report, no date] Available at: http://www.trafitec.dk/pub/Road%20safety%20and%20percieved%20risk%20of%20cycle%20tracks%20and%20lanes%20in%20Copenhagen.pdf

But isn't the survey rather incomplete?

J Thorne — 2010-02-09T13:29:20Z

Perhaps we could have a response to the most obvious source of a negative review of the column.

I tend to agree that the omission of the Copenhagen studies of before-and-after infrastructure installation tends to reduce the credibility of the paper and that there is some confusion regarding just what is considered "vehicular cycling."

Healthy Worker Effect among ex-asbestos workers: A prevalence study

V Murlidhar — 2009-12-01T15:04:38Z

Healthy Worker Effect among ex-asbestos workers: A prevalence study
V Murlidhar
Occupational Health and Safety Centre, Mumbai, India.
6, Neelkant apts, Gokuldas Pasta Road, Dadar (E),
Mumbai, 400014. India.
www.ohscmumbai.com

The study identified those suffering from Asbestosis (parenchymal and pleural non-malignant disease) among the permanent workers of the Hindustan Composites Factory [1]. The prevalence rate of Asbestosis in study was 23%, which was less than the expected prevalence among workers exposed to asbestos for more than 20 years[1].The primary reason suggested for the lower prevalence was the “healthy worker effect”. Many affected workers had been forced to leave the company or to take voluntary retirement. Some may even have died due to the disease. Hence, the workers remaining in the factory were relatively healthy workers.
During the course of the earlier study we got a list of 648 workers, who had formerly worked with the company. We started to trace the workers over a three year period from May 2006 to April 2009.The residence addresses of several workers had changed as they had to move due to drought conditions in Maharashtra State and also due to the pressures of privatization and globalization. Many workers had since died and many were living in areas that were difficult to access. Of the 648 ex-asbestos workers, we were able to trace 462 workers. Of these 462 workers, we could obtain chest radiographs and perform lung function tests in 385 workers.
We found that 114 ex-workers had Asbestosis. The prevalence rate of Asbestosis among ex-asbestos workers was 33%, in contrast to the 23% prevalence rate recorded in the study of active workers in the same factory[1].
The primary reason suggested for the low prevalence in the study was the “healthy worker effect”. Many affected workers had been forced to leave the company or to take voluntary retirement (VRS). Some may have died due to the disease. Hence, the workers who remained in the factory were relatively healthy workers[1]. This hypothesis is proved by the analysis of supplementary data.
Though a few studies have been conducted among ex-asbestos workers [2-6], there has been no study of the prevalence of Asbestosis among ex-asbestos workers in India.
Ex-asbestos workers live in the community and many have difficult access to medical facilities. Even if they get access to a medical facility, their disease is rarely diagnosed.
One of the reasons is that doctors are poorly trained in recognizing and diagnosing occupational diseases [1, 7-9]. Occupational disease is taught as part of the much-maligned subject of Community Medicine. Additionally, most colleges do not have ILO radiological plates, which is mandatory for diagnosis. These plates used for comparing the patients’ X-ray with a standard are not available even in top medical colleges in India. Also there is no post-graduate degree in occupational health in any of the major medical colleges in India. The ILO plates are difficult to procure and are costly and hence, medical students and doctors are totally unprepared to diagnose asbestosis. Consequently even a first ranking radiology physician cannot diagnose asbestosis. He invariably certifies the X-ray as normal [1, 7-9].
The ILO plates are used as study material in some institutes like Central Labour Institute (CLI) that give a diploma in Occupational health. But, the candidates chosen to attend the courses are mainly industry appointed doctors who learn it in order to arm themselves to argue against genuine asbestosis cases. Though any registered medical practitioner in India is legally eligible to diagnose Occupational diseases like Asbestosis, they have a faulty impression that they have to be an expert in order to diagnose it. As a result, there are very few unbiased medical doctors willing to diagnose occupational diseases keeping in mind the context of the industrial workplace and the workers’ rights [1, 7-9]. The Industry clearly has an interest in maintaining the status quo that provides little practical recourse to workers to claim their rights, especially given the high labour surplus in the country.
The attitudes of both doctors and other relevant professionals in diagnosing Asbestosis are also influenced by a bias among the professional class against blue-collared workers in general[1, 7, 9]. At times, this leads to medical professionals deliberately misguiding workers who come to them with occupational and environmental health problems related to asbestos[7].
In addition to the problems in diagnosis and access to medical facilities, issues of labour migration and rural poverty make it imperative that the government takes an active role in the finding ex-asbestos workers, educating them about their rights and helping them avail of these rights. Many of the workers live in remote rural areas and they are forced to frequently change their residence due to the economic adversities caused by privatization and globalization from which they have no social welfare-net protection. This makes it very difficult for voluntary organisations like the OHSC to trace all the listed workers. The efforts will continue but we recommend that the State Government should trace all these workers and get them diagnosed and compensate them as per the Law.
We found a much higher prevalence of Asbestosis among ex-asbestos workers as compared to an earlier published study of active workers from the same factory[1]. This proves the hypothesis of the “healthy worker effect” which was suggested as one of the reasons for a lower prevalence in active workers.
There are less than 30 cases of Asbestosis compensated in India among the 100000 exposed workers. Many must have died of the disease or of lung or pleura cancer. Workers involved with asbestos are to be medically checked by the management every year while continuing in such a job and after he has ceased to work in such a job[1]. This is a specific responsibility of the employer in any factory having any hazardous process. All the workers who have left the place of employment with asbestos exposure, under a voluntary retirement scheme or otherwise, need to be medically checked, once a year at the very least[1]. This is their legal right.
This brings to light the urgent need for measures to protect the workers even after they have finished employment in a hazardous facility. By describing the context of occupational health and safety in India, this supplementary data further underscores the higher vulnerability of ex-asbestos workers in the context of forced labour migration and shows that the current environment is insufficient to protect workers from Asbestosis and highlights the need for the Government to take active steps in protecting the health and safety of workers.

References

1. Murlidhar, V. and V. Kanhere, Asbestosis in an asbestos composite mill at Mumbai: A prevalence study. Environ Health, 2005. 4(1): p. 24.
2. Carnevale, F., [Early retirement for ex asbestos workers. The role of the National Insurance Institute for work Accidents]. Epidemiol Prev, 2000. 24(3): p. 132-4.
3. Ciapini, C., et al., [Health intervention in ex-asbestos exposed workers according to the Toscana region operative guidelines]. G Ital Med Lav Ergon, 2003. 25 Suppl(3): p. 131-2.
4. Jones, R.N., et al., Progression of asbestos effects: a prospective longitudinal study of chest radiographs and lung function. Br J Ind Med, 1989. 46(2): p. 97-105.
5. Luisi, V., et al., [Health surveillance of subjects formerly exposed to asbestos in Puglia]. G Ital Med Lav Ergon, 2006. 28(2): p. 166-8.
6. Tulchinsky, T.H., et al., Cancer in ex-asbestos cement workers in Israel, 1953-1992. Am J Ind Med, 1999. 35(1): p. 1-8.
7. Mudur, G., Asbestos poisoning was covered up by doctors, claims health team. BMJ, 2003. 327: p. 248.
8. Murlidhar, V., Occupational health physicians: unwilling or unable to practise ethically. Indian Journal of Medical ethics, 2002. 10: p. 26.
9. Murlidhar, V., Demystifying Occupational and Environmental Health: Experience from India, in Science and Citizens: Globalization and the Challenge of Engagement, M. Leach, I. Scoones, and B. Wynne, Editors. 2005, Zed Books: London, UK. p. 130-141.

Authors' response to Morten Lange's comments

Conor Reynolds — 2009-12-01T15:00:53Z

We thank Morten Lange for his comprehensive and thoughtful comments about our literature review. We are pleased that the article is of interest to the wider community of cycling advocates as well as academics who study cycling safety. The points made by Mr. Lange offer valuable insights into the challenges of increasing cycling rates, and the need to promote bicycling because it has a low-impact on the environment and is a sustainable mode of transportation. In general, and as the title so-alludes, we chose to constrain the scope of our literature review to topics directly related to the influence of physical infrastructure in the built environment, rather than expand it to include detailed discussion about regulation (e.g. pros and cons of helmet legislation), or cyclist education (e.g. cyclist skills courses and vehicular cycling).

However, we would like to respond to three of the issues raised: first, whether we have overemphasized the risk of crashes and injury to the detriment of the health benefits of cycling; second, whether helmets reduce injury rates; and third, vehicular cycling.

First of all, we agree that there are many health benefits of cycling and have outlined them at the beginning of the article. Mr. Lange suggests that our article may be interpreted as blaming and worrying the victim by focusing on cycling safety. This is certainly not our intent. The injury rate data in different jurisdictions clearly illustrate that cyclists in North America face a risk of injury that is several times higher than in many European countries. Our motivation for performing this review and encouraging further study is the belief – supported by the evidence – that through concerted action by various stakeholders, cycling can be made safer in all jurisdictions.

Secondly, we agree that D. Robinson’s statistical analyses of helmet use and injury reveal that regulation of helmet use does not necessarily result in a significant reduction in serious head injury on a population basis [1]. She highlighted that the number of people cycling in the region studied decreased after introduction of such laws. We cited her article in our review specifically to illustrate that helmet legislation can discourage cycling. In contrast, improvements to infrastructure could both improve safety and make cycling more attractive. However, we could not support any assertion that helmets do not protect individuals from serious injury: they do. Modern cycling helmets are effective at preventing head injuries including skull and brain injury in head impacts against a vehicle or against the ground. Biomechanical testing using artificial head forms in matched drop tower impacts has clearly established the efficacy of helmets on an individual basis. Indeed, based on the reduction in head accelerations, these tests have shown that a head impact that would result in permanent debilitating brain injury (such as a person living their life out in a vegetative state) in a cyclist not wearing a helmet can be reduced in severity to an impact that would cause only a mild concussion or no concussion at all in a cyclist who is wearing a helmet [2, 3]. Case-control studies have also definitely established that helmets are effective at preventing head injury in real-world head impacts [4]. We encourage all cyclists to wear bicycle helmets while cycling for the clear and obvious benefits outlined above. Our focus on infrastructure was intended to address the issue of primary prevention, rather than to discourage measures to reduce injury severity.

Third, we are indeed aware that there is an outspoken group that advocates for vehicular cycling. As we understand it, they advocate that cyclists should have the same access to the road network as motorized vehicles, in part because they believe that cycling on roads is safer than on other transportation infrastructure. Policies about access to the road network were not a subject of our review. Laws in most North American jurisdictions specify roads as the location for cyclists, and often forbid cyclists on sidewalks. Safety related to various types of transportation infrastructure was the focus of our review. In comparison to cycling on sidewalks and on multiuse paths, on-road cycling appears to be safer. In comparison to cycling on bicycle-specific infrastructure (paths, lanes, routes), on-road cycling appears to be less safe.

Finally, we would like to mention that all of the authors have been enthusiastic cyclists for many years, and have cycled in many countries around the world. We are optimistic that with continued efforts by cycling advocates and academics, cycling rates will increase in the coming years while their risk of injury is further reduced.

C. Reynolds, M. Harris, K. Teschke, P. Cripton and M. Winters

References

1. Robinson DL: No clear evidence from countries that have enforced the wearing of helmets. BMJ 2006, 332:722-725.

2. Benz G, McIntosh A, Kallieris D, Daum R: A biomechanical study of bicycle helmets' effectiveness in childhood. Eur J Pediatr Surg 1993, 3:259-263

3. Scher I, Harley E, Richards D, Thomas R: Likelihood of brain injury in motorcycle accidents: A comparison of novelty and DOT-approved helmets. SAE World Congress 2009, 2009-01-0248

4. Thompson DC, Rivara FP, Thompson R: Helmets for preventing head and facial injuries in bicyclists. Cochrane Database Syst Rev. 2000, (2):CD001855.

Some caveats: Relative risk, Perceived risk,Helmet efficiency, Training

Morten Lange — 2009-12-01T14:59:58Z

Thanks to the authors for carrying out such a large review of the research literature on roads/facilities and cycling safety, and bringing forth some of the multitude of arguments for increased cycling for transport.

I have several caveats though, many of which are shared with many that have put some long-term effort into understanding the issues and myths around cycling for transport. As such they should be known to the authors, as this is mostly readily available to those interested. This time around I'll mention them rather summarily :

A. This article is not primarily of academic interest, rather the connection to key concerns in society is spelled out in the article, and the authors seem to hope to bring an important piece to a puzzle helping society to provide better for cyclists to improve their safety. So the preconceptions that the authors build on and the mindset in which the article will be read are important.

B. Reading the introductory paragraphs it seems that the preconception of cycling being "inherently" dangerous is shared by the authors, as it will probably be by most readers. But to what extent does this preconception hold true ? The prime statistic that has been used to underpin the unsafe nature of cycling is to compare injuries pr. kilometre or mile with that of travelling in an car. But, as detailed in the 1999 EU booklet, "Cycling the way ahead for towns and cities", referring to various studies, this is misleading. As an example pedestrians have more deaths pr. kilometre than cyclists, and cyclists have a comparable number of deaths as do car occupants. Also on a per-trip basis. For certain age-groups, risk is much lower on bicycles than in cars.
Another thing is this all "conveniently" excludes the question of the counterpart. Saying cycling is dangerous because cars drive fast and are large and heavy is like... ( Insert favourite victim-blaming phrase here ).

Besides cyclists live longer than non-cyclists, according to several studies. That does not diminish the importance of improving safety for cyclists, but should put cause-and-effect pondering into perspective. Cyclists do not die because of cycling, or because of being vulnerable, they die because of excessive speeds of cars, taking size, weight manoeuvrability and lack of criminalisation of dangerous behaviour into account. Instead of takling of vulnerable road users, which sets them out as 2the others" we should talk of them as users of healthy means of transport. "Sound road users" ?

C. The article gives the impressions that safety needs to be improved to increase cycling. The above should make the point that safety is not so bad. The difference is who is to blame for lack of safety. Unlike car users the threat comes from another group of users, that by the way also pollute, restrict access, and crave vast resources and areas of land.
But clearly there is a problem of perceived risk. And clearly for many cyclists, especially novice ones, the feeling of being unsafe is a serious impediment.

D. when talking of safety it is important to bear in mind that traing for cyclists, as well as years of experience both builds,trust, improves safety and inspires to growth in cycling which can bring about increased safety, not least through heightened awareness amongst motorists.

E. The article seems to seek to shift focus in cycling safety from helmets etc to facilities. To shift focus from helmets is laudable, as their efficiencies have been much overstated, and are a hassle to many new and seasoned cyclists. And focus on helmets for cyclists generally constitute victim blaming in the case of collisions with cars.
But in quote ii below the authors misrepresent the facts on helmet efficiency in the eyes of many experts. Anyone with god quality studies not mentioned in the Wikipedia article on bicycle helmets is encouraged to add references and a two-sentence synopsis in the appropriate paragraph. Probably unwittingly the authors of the present article (indirectly) misrepresent the main conclusion of one of the authors they cite. The conclusion of Dorothy Robinson, senior statistician, is not that helmets work, but that compulsion can reduce cycling. Her conclusion from several studies, are that helmet compulsion that brought about a very significant change in helmet usage in several jurisdictions, was not accompanied by any detectable improvement in the risk of serious head injuries. The reduction in cycling, following the enforcement of the helmet compulsion laws was however clear and significant.

E. Finally I miss at least a short reference to the contrarian arguments to Pucher et al, that is the concept and the arguments for "Vehicular cycling", which appears as a word in the tables, but is not explained nor countered. See e.g John Franklin (Cyclecarft.co.uk) that wrote the book used for the national cycle training standard in the UK, John Forester etc.

Best Regards,
Morten Lange, MSc in Physics, Reykjavík, Iceland

Relevant quotes from the article:
i) "Bicyclists are vulnerable because they must frequently share the same infrastructure with motorized vehicles, and yet bicycles offer their users no physical protection in the event of a crash. In addition, the mass of a typical automobile is at least an order of magnitude greater than a bicycle plus its rider, and motorized vehicles have top speeds that are considerably faster than bicycles. As a result, bicycle riders who are
involved in a crash are exposed to a much higher risk of injury compared to motor vehicle users (with the exception of motorcycle riders)."

ii)
"While helmets are effective in reducing the severity of head injuries, they do not address impacts to other parts of the body [16, 17]. More importantly, they do not prevent incidents from occurring in the first place [18], and legislating their use may even
discourage cycling [19]."

Biphasic model for chromosome aberrations in barley seeds

Alfred Koerblein — 2009-03-17T12:43:51Z

Dear Dr Dropkin

I used your biphasic model ERR~f(dose,beta,sigma,tau) for chromosome aberrations in barley seeds (see Geras'kin SA, Oudalova AA, Kim JK, Dikarev VG, Dikareva NS. Cytogenetic effect of low dose gamma-radiation in Hordeum vulgare seedlings:
non-linear dose-effect relationship. Radiat Environ Biophys. 2007 Mar;46(1):31-41.) Your model fits these data perfectly well. I determine a value of R of 8.4.
If you are interested in my analysis just contact me (alfred.koerblein@gmx.de).

Best regards,
Alfred Koerblein