March 2003 Newsletter - MEDICHEM



Medichem 2003 Board Elections – Call for Candidates

This year, the Medichem Board member Miroslav Cikrt arrives at the end of his term of office. Thus, one seat on the Medichem Board is to be distributed.

Prof. Cikrt has stated that for personal reasons he is not able to stand as a candidate again for a further term of office.

You, Medichem members in good standing, are now asked to nominate candidates for the Board, if you want to do so.

According to Article 5 Sect. 4.1 of the Medichem Constitution, each Board member shall be from a different country. This rule does not apply for those holding the offices of Chairman, Vice Chairman, Secretary, Treasurer, and immediate Past Chairman.

This year, candidates for Board membership must not be from Argentina, Austria, Bulgaria, Canada, France, Germany, India, Poland, South Africa, Taiwan, The Netherlands, United Kingdom, or USA.

All candidates must be Medichem Members in good standing, and also ICOH members in good standing, or at least agree to join ICOH if elected. Furthermore, the nomination shall only be valid if it is sent in along with written acceptance of the nomination from the candidate himself or herself. Nominations must be sent to the Secretary of Medichem, Dr. Michael Nasterlack, by mail or fax (please note the secretary's new fax number on the right side of this page). They must be in possession of the secretary no later than May 31st, 2003.

The ballot form for the election will be sent out along with the next Newsletter in July 2002.

Dr. Michael Nasterlack

(Ludwigshafen, Germany)

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Minutes of the Medichem General Assembly, Tuesday, February 25th, 2003,

Hotel Bourbon, Iguassu Falls, Brazil

Present: 20 members in good standing (quorum needed for decisions: 30)

Chairman Stephen Borron opened the meeting at 18:45 pm. Following a proposal by Board Member Friedrich Schmahl, these Members who newly joined Medichem since the last General Assembly introduced themselves to the audience. Continued on pg 2

Honorary President:

Prof. Dr. med. Dr. h.c. Alfred M. Thiess

Chairman:

Dr. Stephen W. Borron

International Toxicology Consultants, LLC

1025 Connecticut Avenue NW,

Suite 1000

Washington, DC 20036-5417 (USA)

Phone: +1-202-588-0620

Fax: +1-202-478-0444

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Secretary:

Dr. Michael Nasterlack

BASF AG

GOA/C, H 306

D-67056 Ludwigshafen (Germany)

Phone:+49-621-60 42833

Fax: +49-621-60 43322

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Treasurer:

Dr. Andreas Flückiger (Switzerland)

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Board Members:

Dr. P.J. Boogaard (Netherlands)

Prof. M. Cikrt (Czech Republic)

Dr. R. Garnier (France)

Dr. J. Ger (Taiwan)

Dr. S.S. Guirguis (Canada)

Prof. O. Jahn (Austria)

Prof. T. Popov (Bulgaria)

Dr. T. Rajgopal (India)

Prof. K. Rydzynski (Poland)

Dr. F.G. Rose (U.K.)

Dr. S.O. Salomon (Argentina)

Prof. F.W. Schmahl (Germany)

Dr. H. van der Merwe (South Africa)

Dr. Leslie M. Yee (USA)

TOP 1: Approval of agenda for the 2003 General Assembly

The agenda as distributed by the Secretary was accepted without further amendments.

TOP 2: Approval of the minutes of the 2002 General Assembly in Baltimore

The minutes as published in the November 2002 Medichem Newsletter and sent out to all Members by Secretary Michael Nasterlack were accepted without amendment.

TOP 3: Chairman's report

As all important activities of the Chairman are covered by agenda items later in the meeting, no formal report was presented at this time.

TOP 4: Treasurer's report

Andreas Flückiger reported that with expenditures amounting to CHF 34,628.05 and revenues of CHF 47,801.30, the fiscal year 2002 ended with an increase of Medichem's assets of CHF 13,173.25. To date, 75 members have not yet paid their dues. MN will contact these ones and try to figure out whether there is any further interest in their Medichem membership. Medichem's individual membership fees presently amount to less than the fees collected from eleven sustaining members. The credit balance on December 31st, 2002 was CHF 194,810.10 (US $ 139,150.07 at the exchange rate on that day). CHF 100,495 are in a certificate of deposit which has a higher interest rate than the normal bank account. Although Medichem's assets appear to have grown again since the last report, some expected invoices had not yet arrived in 2002 and will only be booked in 2003. AF expects a moderate deficit by the end of 2003 which will approximately make up for the past year’s gain and thus will leave the two years balance unchanged.

The books were revised by Medichem’s honorary Member Walter Urbatus and found to be in good order. Chairman Stephen Borron expressed the Board’s appreciation for the work done by the Treasurer. The General Assembly expressed their thanks to Andreas Flückiger, Walter Urbatus and the Treasurer's wife Marta for their ongoing good work in connection with the Medichem chest with a warm applause.

TOP 5: Secretary's report

Michael Nasterlack gave a short update on the development of Medichem's membership during the past four months. From November 2002 to February 2003 Medichem had lost 2 and gained 12 members, the present headcount is 304 from 42 countries. However, as anticipated in the last report and mentioned above, Andreas Flückiger provided a list of 54 "silent members", and we will have to consider most of them lost to Medichem.

Since October 2002 MN issued 1 Newsletter. The revision of the Medichem Handbook is currently underway and will be sent out to the members together with the March 2003 Newsletter. All costs for printing and distribution were borne by BASF Aktiengesellschaft Ludwigshafen.

The question was discussed whether the Newsletter should be distributed electronically in the future in order to save time and costs. However, a limited number of issues would have to be printed and posted anyway to reach the Medichem members without internet access or e-mail account. Thus, the additional expenditure to to keep records on whom to send paper or not might well outweigh the expected savings. Any member, however, who for any reason does not wish to receive paper copies of the Newsletter, should please feel free to advise the secretary so.

For the ISSA International Symposium in Frankfurt (Germany) in May 2003 Medichem was asked to find one and in fact will be able to provide two speakers. This was gratefully acknowledged by ISSA through explicitly naming Medichem as a supporter of the conference in the final programme.

TOP 6: Implementation of Medichem/ACOEM MOU

Board Member Frank Rose has raised several points and made several proposals in an e-mail to the Board. It is understood that the participation in this MOU is purely voluntary. Members will be asked directly, new members will find a respective question on the application form. To enable the identification of relevant experts it is proposed to use the same coding as ACOEM for expertise. Questions of legal responsibility will have to be settled between participants and their respective employers. Frank Rose hopes to set up the basis for the system by the middle of this year. As soon as it works, relevant parties such as national poison centers can be contacted and be made aware of the system. The methods of contact in case of emergency still need to be clarified. There is consensus that the system will not be accessible to the general public. The General Assembly expressed their gratitude to Frank and his task force for their good work.

TOP 7: Update on preparation of Medichem Congresses 2004 – 2005

Stephen Borron and Robert Garnier will organize the XXXII Medichem Congress 2004 in Paris/France. It will probably take place in the first week of September (will be decided by the end of April).

Shrinivas Shanbhag, the National Representative of India, and Thirumalai Rajgopal offered to host the XXXIII Medichem Congress 2005 in Goa/India. The anticipated date will be September 2005. Eventually there will be a cooperation with the Indian Association of Occupatonal Health (IAOH). The first announcement for this congress could be sent out by the end of 2003. The General Assembly welcomed this offer with warm applause.

TOP 8: Report on public relations for Medichem by OD Systems

Stephen Borron reported that OD Systems had provided a draft report shortly before the meeting. It has been handed to the Board Members just two days ago. A working group consisting of Stephen Borron, Frank Rose, Hans van der Merwe and Javier Amherd is going to review the proposals and prioritize the implementation. The final report will contain an implementation plan as well. The Medichem Membership will be informed about the final report along with one of the next Newsletters.

TOP 9: Miscellaneous

There is an increased need to get the word out on Medichem. To this end, the Medichem website where Noel Humphry and his assistant Kerry Campbell have done an outstanding job will be further improved through enhanced features such as a discussion forum, a restricted members only zone, etc. Noel and Stephen will co-operate on how best to proceed in managing the website.

The Board and the General Assembly thanked Sergio Salomon for his good work in organizing this year's Mini-Symposium with a big round of applause.

The Chairman adjourned the meeting at 19:30 p.m. The next General Assembly will be held in Paris (see TOP 7). The exact date and venue will be communicated.

Dr. Michael Nasterlack

Ludwigshafen (Germany)

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Brussels Announces Laws to Cut VOCs in Paints and Refinishes

The European Commission has announced draft legislation to reduce volatile organic compound (VOC) content in decorative paints and varnishes for professional and private use, and in car refinishes, by about 50 %, or 2800,000 m.t./year. The proposed laws will set Europe-wide limits on solvent content in those products for the first time. Limits to VOC content in decorative paints and varnishes will be cut in two phases, ending on January 1, 2007 and January 1, 2010, under the legislation. VOC content in car refinishes must be cut in one phase, ending 2007. The estimated cost of the changes to the paints industry is €108 million-€57 million ($114 million-$165 million)/year, but the estimated benefits in terms of improved air quality are more than € 580 million/year, the commission says. The commission has been preparing the legislation for more than two years.

It builds on laws the commission introduced in 1999 reducing VOC content in industrial paints and coatings, excluding car refinishes.

Europe's coatings industry says it has been switching from solventborne to waterborne products in anticipation of tougher environmental legislation. Cuts in VOC content from current levels will likely affect the quality of decorative paints, however, the industry says. "Paints will not maintain the required performance," says European paints industry association CEPE (Brussels).

The industry welcomes harmonization of European Union (EU) laws, however. "We welcome the prospect of EU legislation to replace a patchwork of national rules," says Jacques Warnon, technical director at CEPE. VOC emissions contribute to the formation of ground-level ozone (smog), one of the big air quality problems in the EU, the commission says. "The commission is committed to cleaning up the air that Europeans breathe, and this is part of our efforts to deliver what we have promised," says European environment commissioner Margot Wallström.

EU member states committed in 2001 to national emission ceilings of materials such sulfur dioxide, nitrous oxide, and VOCs, which will come into force in 2010. The recently announced paints legislation" will provide member states with a new tool to comply with the requirements to limit national emissions that they have signed up to," Wallström says.

Dr. Michael Nasterlack

Ludwigshafen (Germany)

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Salient issues from the 3rd International Symposium on Silica, Silicosis, Cancer and Other Diseases and Comments on Progress since the 2nd Symposium in 1993

This October symposium added substantially on the information base developed at the second which I attended in San Francisco in 1993 and for which I also prepared a summary. The gist of my 1993 report was that some exposures at a level half that of the then and current standard had been found to cause silicosis, that cases with exposures within the standard tended to occur after decades of exposure, and that lung cancer had been found regularly in exposed workers but the cases were largely found in silicotics and that prevention of silicosis might prevent lung cancer. Absent at both meetings and in the literature were studies looking for lung cancer in exposed non-smokers. In 1993, it was well understood that silica caused silicosis in non-smokers and that smoking potentiated the silicotic process. There also was a general feeling that prevention of silicosis could prevent, or at least largely prevent, lung cancer. That concept is no longer secure.

I followed the scientific literature quite closely from 1993 to 1995 at which time I began tracking silica hazards only as they appeared in my regular scientific reading and conference attendance. Within the latter scope, the Stockholm International Conference on Occupational Medicine in 1996 included a number of interesting presentations on silica. Excess lung cancers were reported in employees with International Labor Organization (ILO) ILO-1 X-ray readings but without silicosis and a specific locus on the P53 gene of lung cancers from silicotics also was reported. A similar finding on a separate locus in that gene had previously been found in lung cancers of smokers in the general population.

Those two conference papers proved prescient as the International Agency for Research on Cancer (IARC) determined that silica was a known human carcinogen several weeks later. Following IARC's action, the Chemical Manufacturing Association acted as a sponsor for a meeting for companies with employees exposed to silica. Analysis at the meeting pointed up IARC's careful hedges in their determination. IARC had noted the absence of a dependable dose/rate (d/r) response between exposures and cancer, and included a number of qualifying comments. Most attendees appeared to find these qualifying statements as representative of the real situation as I was unable to find anyone else who believed that silica was by itself carcinogenic. I pointed out the findings regarding a specific loci on P53 genes, noting that the initial finding in smokers' lung cancers had been the final straw that lead the chief executive officers of cigarette companies to admit that smoking caused lung cancer. All the same, there were no takers. The chairman of the CMA meeting called me a few weeks later to comment that he had only then realized the impact of these genetic studies.

Attending the 3rd symposium were a representative of the sand industry trade association, epidemiologists with experience with working with industry and government, health and safety staff for companies with exposed workers and interested academic and governmental scientists including the silica project officers who are responsible for coordinating actions toward setting a silica standard for OSHA and EPA. There were no representatives from labor unions or from the Mine Safety and Health Administration (MSHA). Having a reasonable concern for the correct exposure level, their absence was a first in my experience for a seminar of this stature. Most participants expected no change in the MSHA standard of 1 mg/cubic meter.

As in 1993, there were no papers that presented epidmiologic data from non-smoking workers with silica exposure. What is not widely realized is that the risk of lung cancer is so small in non-smokers (I have never seen a case) that no one has obtained a sufficiently large population.

Some thinking at the 3rd symposium remained similar to the second in that populations will continue to develop silicosis at levels within current standards to include the German MAK value of 1.5 mg/cubic meter, which is 50% above ours. Conversely, data at the 2nd and 3rd meetings reflected a few populations that showed no adverse effects at 1 mg/cubic meter. Close attention to progress in silica toxicology just before and since the IARC determination explains the basis for their qualifying statements, i.e., that variations of complex factors in the silica particle from one workplace exposure to another explain these differences.

Some of these factors such as heating silica particles to high temperatures or allowing the particles to age for weeks or months after fracturing have long been known to be important in reducing risk of silicosis. In the last several years, attention to the surface of the particle revealed protective or synergistic effects that can blur or overwhelm risk data based on respirable silica alone. Electron microscopic studies of the surface have shown that very rough surface irregularities make the particle more toxic as does the presence of steel from the fractioning machinery or the presence of iron that electron spin trapping microscopy has shown to have an excess of surface radicals. Conversely, most iron contaminants are protective as are clay or aluminum silicate coatings that can be detected by differential electron microscopy, but only by varying voltage levels.

Another powerful influence, not yet corrected for in any study, is genetic distribution of sensitivity to a powerful cancer pathway, tumor necrosis factor. According to W. E. Wallace of NIOSH, based on a small-range finding study, about half of male Caucasians are hyper-susceptible to activation of this factor by silica. In a population exposed to silica resulting in silicosis for some individuals, about ¾ of the cases occurred in the half that was hypersensitive.

Another cancer activating agent, activator protein-1 also is stimulated by silica, typically playing a role via tissue inflammation. Strangely, the effect of this agent was muted in animal cells with an aspirin dose equivalent to one standard (325 mg) tablet three times per day in an adult human.

Data polled from multiple published studies (not just meta analysis of results) has been evaluated since the last seminar. These data have shown a dose rate response (d/r) between silica exposure and silicosis and with lung cancer (the latter with an internal 'not statistical' correction for smoking). This pooled d/r results can be sharpened by eliminating populations that had exposures to non-toxic silica. After an enormous amount of work, the d/r data then may be used to generate risk extrapolations risk for various diseases at the current 1 mg level.

Kyle Steenland of Emory University led this study. He presented risk assessment (R/A) levels showing lifetime population risks of about 1.9% for silica-related death and 1.7% for lung cancer, over 50% for silicosis (defined as an ILO 1 reading or greater) and 1.8% for renal disease. These levels are above those experienced by almost everyone I talked with at the meeting but no one tracked populations to meet the R/A lifetime criteria: 45 years exposure with retirement at 65 and life expectancy (and follow up) to age 80. Steenland's risk assessment of course presumes that a particular workplace will have an average risk as regards surface characteristics. On the other hand, in a population in which the appearance of cases appears to conform to the general epidemiology of silicosis, his assessment should be valid and useful for estimating lifetime risk.

As regards surveillance, ILO chest films remain the gold standard for early detection of silicosis. I talked with a number of physicians who advise management on populations that regularly develop cases of silicosis. None had noticed change in the slope for decline of pulmonary function, particularly FVC as an early warning for the appearance of silicosis in long-term employees with chronic silicosis. All had noted, of course a similar picture with acute silicosis where the reaction is obvious and also immediate with accelerated onset of symptoms with very high exposure situations. These physicians were responsible for surveillance in populations, particularly S. African gold mines, where protection was dependent on poorly used respirators. Such environments currently develop many, sometimes hundreds of, new cases each year. I was unable to find physicians who were dealing with employee groups that presented long-term cases of chronic silicosis, in which the appearance of symptoms was gradual.

Efforts to improve on the PA chest with other imaging techniques for silica surveillance have been futile. On a number of occasions, I have tried to persuade consultants who deal with new cases of ILO-1 or ILO-2 readings that unlike the case for asbestos exposure, the CAT scan is not useful in determining presence of silicosis or determining occupational causation in silica exposure. It does make some pleural plaques apparent in silica-exposed persons, but finding these plaques does not contribute to the determination of silicosis. While I understand that consultants need to be thorough when making a pulmonary evaluation on the basis of ILO readings, that procedure provides no new useful information with silicosis determination or case management. Fortunately for carrying this point to consultants, the lack of utility in CAT scans was underscored by Dr. John E. Parker, now retired from NIOSH but quite active. He also had a mini-series devoted to the ILO's plans for updating the its X-ray coding procedure and a NIOSH training program for B readers.

It is, and has been for some time, the position of the trade association for the sand industry that potentially exposed employees be examined by PA chest examinations every two years with readings by the ILO standard. It also would be fair to say that if the chief executive of the trade association were approached by a manager regarding an employee with an ILO-1/1 (a middle ILO-1 reading) his recommendation would be to remove the employee from further exposure.

My participation in the seminar and a brief review of the literature tells me that any temporary removal of an employee with symptoms of silicosis is of little value. Any symptomatic employee probably has a delayed pulmonary clearance versus fellow employees who never develop symptoms in the same exposure. Participants at the seminar pointed out that the average half-life for pulmonary clearance for insoluble respirable particles is on the order of 400 days. Consequently, a temporary cessation of exposure for a few months is trivial.

I can forward a copy of the symposium proceedings to those who write with their address.. It includes most of the point presentations listed above including that of the silica-related P53 gene. Some authors' presentations are not in the program. Copies of their power point presentations have been requested. One such, Dr. Steenland's just arrived.

Dr. John Dougherty, Leonia (U.S.A.)

P.S. I am very grateful to John Dougherty that he provided this contribution on a pertinent subject. This is exactly what the Newsletter is meant to be: a forum for all members who want to inform about significant issues of general interest to the Medichem community. Thanks John!

Dr. Michael Nasterlack

Ludwigshafen (Germany)

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Ethnic Differences in Clinical Acrylonitrile Intoxication Symptoms?

Acrylonitrile is an important high-volume chemical in the industrial production of polymers. Its toxicity is presently being reviewed by the European Communities, within the process of Risk Assessment of Existing Chemicals. The compound has a high potential for skin penetration, it is of high acute toxicity, and it is carcinogenic in experimental animals.  The toxic properties of acrylonitrile have been related to its metabolism, which proceeds via a glutathione-dependent detoxification pathway on one hand, and, on the other hand, via oxidative metabolism, mediated by CYP2E1, which inter alia leads to cyanide formation. Hence, cyanide antidotes and N-acetyl-cysteine are being viewed as powerful antidotes. Acute intoxication experiments were performed in rats. In this species, cyanide antidotes (DMAP/thiosulfate) proved not effective, but N-acetyl-cysteine was. The experimental clinical picture (lachrymation, salivation, miosis) pointed to significant acetyl-cholinesterase inhibition upon acute acrylonitrile poisoning; this was supported by an experimental antidotal effectiveness of atropine. Published observations of a number of cases of industrial human acrylonitrile.

Intoxications in Germany were in contrast to the experimental symptoms and pointed to an overwhelming importance of cyanide as ultimately toxic metabolite. However, recent reports on clinical symptoms of acrylonitrile intoxications in China did not coincide with the European observations; they pointed to a clinically relevant inhibition of acetylcholinesterase, much consistent with the experimental findings in rats. During the past few years, we have investigated possible gene-environment interactions relevant for acrylonitrile toxicity. On the basis of known genetic and ethnic differences the enzymes metabolizing acrylonitrile (glutathione S-transferases and CYP2E1) a rationale can be deduced for the observed differences in response of European vs. Far Eastern populations. The primary factor seems to be a different range of expression of CYP2E1 enzyme activities. Thus, the relevance of ethnic differences for development of the clinical picture of an acute industrial intoxication is demonstrated for the first time. Potential ethnic differences should therefore be more considered in industrial toxicology.

(H.M. Bolt et al. Lecture given at the 27th International Congress on Occupational Health, Iguassu Falls, Brazil).

Dr. Michael Nasterlack

Ludwigshafen (Germany)

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Annoyance and Performance During the Experimental Chemical Challenge of Subjects with Multiple Chemical Sensitivity

The study explored the subjective reactions and psychological test performance of smell-intolerant subjects during consecutive challenges to chemicals with contrasting neurotoxic properties.

Women with symptoms compatible with multiple chemical sensitivity (N=10) and healthy referents (N=20) were individually challenged in an exposure chamber. All the subjects attended two separate 2-hour sessions of exposure to n-butyl acetate and toluene, in counterbalanced sequence. After an initial phase without exposure, air concentrations were increased in steps ranging from 3.6 to 57 mg/m3 for n-butyl acetate and from 11 to 180 mg/m3 for toluene. The response measures comprised ratings of annoyance and smell intensity and also neurobehavioral test performance.

Both groups showed an increase in annoyance ratings and a decrease in test performance in the initial unexposed chamber phase and also in the first phase of the chemical exposure, these results indicating slight immediate expectancy or "suggestion" effects. During the six chamber phases, the ratings of mucous membrane irritation and fatigue showed a steeper increase in the group with multiple chemical sensitivity than among the referents, while the ratings of smell intensity and smell annoyance were similar in the two groups. A reduction in test performance was observed during the chamber phases, particularly in the group with multiple chemical sensitivity. No relation was found between the ratings or performance and chemical substance.

Stronger immediate expectancy or "suggestion" reactions than normal did not characterize the group with multiple chemical sensitivity. This group showed a stronger than normal gradual build-up of fatigue, mucous membrane irritation, and reduced performance during chemical exposure. The authors conclude that the results offer the most support to an irritative basis for multiple chemical exposure.

(K. Österberg et al., Scand J Occup Environ Health 2003; 29: 40-50).

Dr. Michael Nasterlack

Ludwigshafen (Germany)

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A Review of Epidemiological Studies about the Incidence and Etiological Factors of Cryptorchidism - Relevance to Endocrine-Disrupting Chemicals

Recently, it has been reported that the incidence of male genitourinary abnormalities (such as cryptorchidism) has been increasing because of the presence of endocrine-disrupting chemicals (EDCs) in the environment. This report reviews the papers related to cryptorchidism beginning in the 1960s to clarify the trends in incidence of dryptorchidism and to discuss the association between cryptorchidism and risk factors, including EDCs.

The incidence of cryptorchidism tended to increase in almost researched countries until the mid-1980s, but has shown regional differences since 1990. In Japan, the trend of the incidence of cryptorchidism is unclear because there is no monitoring system for cryptorchidism.

It is necessary to establish both criteria and a monitoring system to research the incidence of cryptorchidism. The risk factors in epidemiological studies include low birth weight, being small for gestational age, a short gestation period, high maternal body weight, the change during pregnancy of maternal hormones (by exposure to diethylstilbestrol DES or estrogen), and exposure to chemicals. However, the associations between children with cryptorchidism and exposure to EDCs as well as between cryptorchidism and exposure to estrogen of the fetus are not clear because very few reports have quantatively evaluated EDCs. It is known that some EDCs act as estrogen receptor agonists and change hormonal mobility as exogenous estrogen. It has also been suggested that hormonal drugs such as DES affect the maternal endocrine system in pregnancy and are associated with the incidence of cryptorchidism. In the future, epidemiological studies that clarify the association between cryptorchidism and EDCs such as daidzein and genistein and the quantitative evaluation of exposure factors using biological materials are necessary.

Prof. Alfred Thiess, Ludwigshafen (Germany)

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Welcome to New Members

Robin August, Nurse Practitioner, Bear (U.S.A.), Prof. Henrique Vicente Della Rosa, Toxikón Assessoria Toxicológica, Sao Paulo (Brazil), Dr. Eric T. Evenson, Procter & Gamble Company, Cincinnati (U.S.A.), Dr. Sibylle Hildenbrand, Institute of Occupational and Social Medicine of the University, Tübingen (Germany), Dr. Simon Madin, ExxonMobil, Southampton (United Kingdom)

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Forthcoming Events

20th International Symposium of the ISSA Chemistry Section 2003

will be held from 22nd to 23rd of May 2003 within the ACHEMA (27th International Exhibition - Congress on Chemical Engineering, Environmental Protection and Biotechnology) in Frankfurt, Germany.

XXXII. Medichem 2004 - Paris

The XXXII. Medichem Congress will take place in September 2004 in Paris. The exact date and venue will be published soon.

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March 2003

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