Environmental Health - Latest Comments

But isn't the survey rather incomplete?

J Thorne — 2010-02-17T00:00:00Z

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."

Authors' response

Conor Reynolds — 2010-02-09T00:00:00Z

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

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

V Murlidhar — 2009-12-01T00:00:00Z

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 — 2009-12-01T00:00:00Z

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 — 2009-12-01T00:00:00Z

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 — 2009-03-17T00:00:00Z

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

Response to Chlorine Institute's Comments

Renee Dufault — 2009-02-11T00:00:00Z

RESPONSE TO CHLORINE INSTITUTE’S COMMENTS

We also share the public’s concern about the safety of our food supply. The order of preference for using chlor-alkali chemicals in HFCS manufacturing was provided by the manager of a high fructose corn syrup plant and stated as 1) mercury cell and then 2) membrane grade. The reason given for the preference stated was that mercury cell caustic enhances “product shelf life.”

A literature review of the uptake of mercury by the corn plant indicated that corn has very low levels of mercury even in soils with elevated mercury caused by sludge application (1, 2, 4, 5, 6). After the steeping step in the HFCS manufacturing process, the de-germing process separates the germ from the endosperm (3). The germ is the portion of the corn most likely to contain any mercury and it is removed at that point of the HFCS manufacturing process while the endosperm is used to produce HFCS (3). So to summarize the results of our literature review, corn feedstock is actually a weak vector for carrying mercury into a wet-mill, and the little that may arrive is separated prior to HFCS production (1-3, 7).

The conclusion we made, that mercury-cell caustic soda could be a likely source of mercury in the high fructose corn syrup samples, was substantiated because other obvious sources of mercury contamination were considered less likely. The Chlorine Institute does not provide any evidence that reassures the public that mercury grade caustic soda is safe to use in food manufacturing processes. The amount of mercury that contaminates the mercury-cell chlor-alkali products is variable and depends on quality control and plant operations. These products, which are used world wide in food processing, have not been adequately regulated. The persistence of mercury in HFCS is a cause for concern. Mercury is considered a neurotoxin in any form. It is interesting to note that Sweden recently banned the use of mercury in any form in any product (8). The Swedish Government's decision on a total mercury ban means that alternative, safer techniques will have to be used in dental care, chemical analysis and the chlor-alkali industry (9).

We agree that most of the caustic soda produced in the United States (US) is now produced by chlor-alkali plants that do not use mercury cell technology. It has been reported that only five mercury cell plants are left - Port Edwards is still operating, although it has committed to phasing out mercury cell technology. Although thousands of tons of mercury pollution could be eliminated annually if these five remaining plants in the U.S. switched to cleaner technology, there are still many more mercury cell chlor-alkali plants operating throughout the rest of the world. The US must lead by example and provide leadership in eliminating this outdated chlor-alkali technology worldwide. In 2006, then Senator Barack Obama introduced legislation to phase out all mercury cell use in chlorine plants by 2012. He re-introduced it in 2007. Earlier in 2008, a version of this legislation also was introduced in the House of Representatives. It's time to pass this legislation.

Sincerely,

Dufault et al
References

1. 1999 -- PUBLIC HEALTH STATEMENT MERCURY CAS#: 7439-97-6
http://www.atsdr.cdc.gov/toxprofiles/tp46-c1-b.pdf

2. 2001 -- Distribution of Mercury in Soil and its Concentration in Runoff
from a Biosolids-Amended Agricultural Watershed
http://jeq.scijournals.org/cgi/reprint/30/6/2173.pdf

3. 1974 -- Heavy Metals in Food Products from Corn
http://www.aaccnet.org/cerealchemistry/backissues/1974/Chem51_779.pdf
4. 2007 -- Heavy Metals (Pb, Cd, As, Hg) Contamination of Edible Grains
Grown and Marketed in Nigeria
http://www.scialert.net/pdfs/rjas/2007/192-195.pdf
5. 2007 -- A note on elevated total gaseous mercury concentrations downwind
from an agriculture field during tilling 1: Sci Total Environ. 2007 Dec 15; 388(1-3):379-88. Epub 2007 Aug 20.

6. 2004 -- Heavy metals in soils and crops in Southeast Asia. 1. Peninsular Malaysia Environ Geochem Health. 2004 Dec; 26(4):343-57.

7. 1983 -- Differential Uptake of Mercury Vapor by Gramineous C(3) and
C(4) Plants Plant Physiol. 1983 Aug;72(4):1040-1042.
8. http://ehstoday.com/environment/hazardous-waste/Sweden_bans_mercury_9872/
9. http://www.sweden.gov.se/sb/d/11459/a/118550

Letter to the Editors Re: Dufault et al. in Environmental Health (2009) 8:2

Arthur Dungan — 2009-02-11T00:00:00Z

February 9, 2009

To the Editors:

While we share public concern about the safety of our food supply, we believe that you did a vast disservice to your readers and the chlor-alkali industry by publishing an article [Dufault et al. in Environmental Health (2009) 8:2] that, without any scientific evidence whatsoever, claims that chlor-alkali plants are the source of the mercury they found in samples of high fructose corn syrup and other food products. The report, “Mercury from chlor-alkali plants: measured concentrations in food product sugar,” carries nothing more than unsubstantiated, unwarranted speculation concerning a purported relationship between such plants and mercury in foods.

While the study raises important questions regarding mercury in the diet, careful evaluation is needed to survey all potential sources and exposures before characterizing a source for consumers’ potential health risk. Simple conjecture born of irresponsible science only serves to misinform and mislead the public. Moreover, deliberate misrepresentation of findings has no role in a peer-reviewed technical journal.

I urge the readers and scientific reviewers of Environmental Health to demand a higher standard of reporting and one that is consistent with research conducted using the scientific method. We are chagrined that the authors of such a study would allow such idle speculation to be prominently reported in the study’s findings. We are outraged that none of the peer reviewers pointed out this obvious speculation or called for changes.

Contrary to the authors’ speculation, it is neither physically nor chemically possible for caustic soda to be the source of the mercury levels identified in this study. The study correctly points out that most of the caustic soda produced in the United States is produced by chlor-alkali plants that do not use mercury cell technology. However, the mercury levels the authors report are some 50 times higher than what can be attributed to any trace amounts of mercury in caustic soda produced by chlor-alkali plants that do not use mercury cell technology.

Food-grade caustic soda is safe to use in the food-processing industry. Caustic soda used in food processing must meet stringent international Food Chemicals Codex standards established by the World Health Organization, Food and Agriculture Organization and international governments. Furthermore, the report fails to account for the possibility of other mercury sources. It is important to note that mercury is ubiquitous in our environment due to natural and man-made sources. For example, it is common to find measurable mercury in the soil in which we grow our food, and the U.S. Environmental Protection Agency allows up to two parts per billion in the drinking water we consume daily.

We urge the editors of Environmental Health and the authors of the study to point out as quickly as possible that they provide no scientific link connecting caustic soda to the reported levels of mercury they found in their study.

Very truly yours,

Arthur E. Dungan
President
The Chlorine Institute, Inc.
1300 Wilson Boulevard
Arlington, VA 22209
Tel: 703-741-5760
Fax: 703-741-6068
www.chlorineinstitute.org

Response to Dr Joffe's coments

Luc Multigner — 2008-08-08T00:00:00Z

We thank Dr Joffe for his comments, with which we largely agree. We have stressed in our publication that the comparative physiology, nature of exposure, development stage at exposure, and a number of ecological factors are of course different between human and rat. These differences must be considered when interpreting wild animals as sentinel species for human health risks. Our study, we feel, makes that abundantly clear, being essentially a prototype in advance of more detailed investigations to come. Concerning testicular cancer, our references to this topic and to the apparent decline in semen quality were made to situate our work in a more general context for readers interested in human reproductive health. We also agree with Dr Joffe that although the influence of substances with endocrine activity is a prevalent hypothesis to explain the worrying trends in male reproductive health, other contributing factors must also be considered [1]

L Multigner, P Kadhel, Ml Pascal, F Huc-Terki, H Kercret, C Massart, E Janky, J Auger,and B Jégou.

[1]Joffe M. Are problems with male reproductive health caused by endocrine disruption? Occup Environ Med, 2001; 58: 281-287

Sentinel species for male reproductive disorders

Michael Joffe — 2008-08-08T00:00:00Z

Dear Sir

Multigner et al. are to be congratulated on their pioneering study on male reproductive parameters both in rats and in humans, comparing those highly exposed to pesticides in a banana plantation with those who are not highly exposed [1]. Their intention to investigate how well rats perform as sentinel indicators for humans is important.

However, their findings cannot be taken at face value, because the two species are not comparable in respect of the developmental stage at which they were exposed to pesticides. One cannot be certain, but it appears that the men were exposed only as adults, whereas it is clear that the rats had been highly exposed at all stages of development as they were conceived in the banana plantation and grew up there. As it is highly likely that the male reproductive system is most susceptible to toxic insult in the early stages of development, their findings of a significantly lower serum concentration of serum testosterone in the rats, but not in the humans, could merely reflect differing stages of exposure, not a species difference. Stage of development at the time of exposure is barely mentioned in the paper, at the end of the penultimate paragraph of the Discussion section.

Another issue is the framing of the problem, which is subject to the vagueness that unfortunately characterises the literature on male reproduction. Early toxic exposure leading to a low adult serum concentration of testosterone could occur by means of any mechanism that reduces the quantity of hormone-secreting tissue in the testis. It does not have to be via an endocrine disrupting mechanism. So why is male reproductive toxicity described from the perspective of endocrine disruption? Even DBCP is described as “not formally identified as [an] endocrine disruptor”, suggesting that this could be its mode of action, when it is a known mutagen that causes dominant lethal mutations [2,3].

Similarly, in the opening paragraph there is the customary reference to the rise in testicular cancer, as if this were relevant to the type of pesticide exposure that is the focus of the study. The rise in this disease, which has been dramatic – at least a four-fold increase in a matter of decades, in a large number of countries – started 100 years ago in continental Europe [4] and even earlier in England and Wales [5]. A large proportion of this increase had occurred before the introduction of any of the modern classes of pesticides (or any suggested endocrine disruptors such as phthalates). Even if pesticides affect the testicular cancer risk [6] they do not come close to explaining the basic epidemiological findings.

Returning to the question of sentinel species, one of the puzzles of testicular cancer is that no satisfactory animal model has ever been found, despite the high degree of conservation of the male reproductive system in mammalian evolution.

Yours sincerely

Michael Joffe

PS: the references need checking – some authors’ names are mis-spelt, and several other details are wrong.

References

1. Multigner L, Kadhel P, Pascal M, Huc-Terki F, Kercret H, Massart C, Janky E, Auger J, Jégou B. Parallel assessment of male reproductive function in workers and wild rats. Environmental Health, 2008; 7: 40.

2. Whorton MD, Foliart DE. Mutagenicity, carcinogenicity and reproductive effects of dibromochloropropane (DBCP). Mutat Res 1983; 123: 13-30.

3. Ryu J-C, Kim Y-J, Chai Y-G. Mutation spectrum of 1,2-dibromo-3-chloropropane, an endocrine disruptor, in the lacI transgenic Big Blue Rat2 fibroblast cell line. Mutagenesis 2002; 17: 301-07.

4. Bergström R, Adami H-O, Möhner M, et al. Increase in testicular cancer incidence in six European countries: a birth cohort phenomenon. J Natl Cancer Inst 1996; 88: 727-33.

5. Davies JM. Testicular cancer in England and Wales: some epidemiological aspects. Lancet 1981; i: 928-32.

6. Hardell L, van Bavel B, Lindstrom G, Carlberg M, Dreifaldt AC, Wijkstrom H, Starkhammar H, Eriksson M, Hallquist A, Kolmert T. Increased concentrations of polychlorinated biphenyls, hexachlorobenzene, and chlordanes in mothers of men with testicular cancer. Environ Health Perspect 2003; 111: 930-34.