On the use of different measures of exposure-experiences from a case-control study on testicular cancer and PVC exposure.

Associations between exposure to PVC plastics and testicular cancer have been reported. To improve the exposure-response analysis in a matched case-control study on testicular cancer and occupational exposures, a self-administered exposure questionnaire and expert assessment was applied and different exposure measures were developed. The questionnaires regarding work histories and employment in PVC production, manufacturing, and handling of PVC products were completed by 1582 subjects (90%). By expert assessment, 360 subjects were considered exposed, and the exposure intensity to PVC plastics for different working periods was determined. Different exposure measures to PVC plastics were then developed, such as ever/never exposed, duration, maximum intensity, median intensity, and cumulative median intensity. The correlation between the different measures of exposure was high for exposure duration and the cumulative median exposure intensity (Spearman rank coefficient r(s) = 0.94), as was the correlation between the maximum intensity and the median intensity (r(s) = 0.94). The agreement between the answers in the questionnaire and the expert assessments was moderate, Kappa value 0.56. The odds ratio for "ever" exposed based on the exposure as reported in the questionnaire was 1.1 (95%, CI 0.82-1.56), and as determined by expert assessment 1.3 (CI 1.05-1.69). The odds ratios for all four different categories of exposure measures varied between 0.86 and 2.6 but decreased by increasing exposure. An overall excess of testicular cancer for the PVC exposed vs. the unexposed was not supported by the pattern seen in a standard exposure-response analysis based on several exposure measures. The findings stress the importance of using several exposure measures as dose surrogates when the underlying toxic mechanisms are unknown and when there are indications of an overall effect.

Testicular cancer and occupational exposures with a focus on xenoestrogens in polyvinyl chloride plastics.

In a case-control study of 148 cases of testicular cancer and 314 healthy controls information was collected on lifetime working histories and specific exposures. The main finding was a six-fold increase in the risk for seminoma, one type of testicular cancer, among plastic workers exposed to polyvinyl chloride (PVC). No overrisks were observed for other plastics than PVC. There may be an aetiological link to xenoestrogens, i.e. chemicals in the environment with oestrogenic properties. Phthalates are used in PVC as plasticizer and have oestrogenic properties that could promote the growth of endocrine sensitive tumour cells. However, this "endocrine disruptors" hypothesis must be further evaluated in experimental models with regard to the causative mechanisms of the oestrogenic tumour promotion.

Sudden infant death syndrome: a possible primary cause.

The hypothesis that poisoning by phosphines, arsines and stibines might be the primary cause of sudden infant death syndrome (SIDS) was investigated. Most mattress materials contain phosphorus or antimony compounds as fire retardant additives. Mattress materials in areas affected by the warmth and perspiration of the sleeping infant were found to be naturally infected by the fungus Scopulariopsis brevicaulis which is thought to be capable of generating phosphines, arsines and stibines from materials containing phosphorus, arsenic or antimony compounds. These gases may cause anticholinesterase poisoning and cardiac failure in infants, but contributory factors include the prone sleeping position and overwrapping. In England and Wales, the progressive increase in SIDS between 1951 and 1988 seems to be related to increasing use of phosphorus and antimony compounds as fire retardents in cot mattresses.

[Neurologic and psychiatric disorders in vinyl chloride disease]. / Neurologische und psychiatrische Störungen bei der Vinylchlorid-Krankheit.

A literature review and an own case observation of neurological and psychiatrical disturbances in vinyl chloride disease are presented. In acute vinyl chloride intoxication, patients complain of vertigo, nausea and headache. At higher concentrations, vinyl chloride exerts a narcotic effect. In patients with chronic occupational exposure, neurological disturbances include sensory-motor polyneuropathy, trigeminal sensory neuropathy, slight pyramidal signs and cerebellar and extrapyramidal motor disorders. Psychiatric disturbances present as neurasthenic or depressive syndromes. Sleep disorders and disorders of sexual functions are frequently encountered. Pathological EEG alterations can be found in a high proportion of patients. The long term course and prognosis of the neurological and psychiatrical disorders in vinyl chloride disease are obscure. In an own case, a slight sensory polyneuropathy, bilateral hyposmia, a marked neurasthenic syndrome, typical EEG changes and computed tomography signs of cerebral atrophy were found in a 56-years-old patient as late as 16 years after the exposure to vinyl chloride.

Acute health effects among firefighters exposed to a polyvinyl chloride (PVC) fire.

Firefighters are frequently being called on to fight fires that are chemical in nature. In the aftermath of a chemical fire in Plainfield, New Jersey on March 20-21, 1985, the authors conducted a retrospective cohort study which surveyed 80 firefighters exposed to burning polyvinyl chloride (PVC) as well as 15 nonexposed firefighter subjects. By means of an 81-item symptom checklist, exposed firefighters reported more frequent and severe symptoms at 5-6 weeks post incident. This was true for a total symptomatology score as well as 19 individual items. Some of the items with an elevated risk were consistent with exposure to hydrogen chloride, the main pyrolysis product of polyvinyl chloride. Other items with an elevated risk appeared to be related to smoke inhalation while others seemed psychosocial in nature. Analyses conducted within the exposed firefighter group showed that fighting the fire the first day, being a truckman, and residence within 1 mile (1.6 km) of the firehouse were significant risk factors for high total symptom scores. These risk factors may have been associated with level or duration of exposure to the toxic substances produced during the fire.

Long-term psychological distress among chemically exposed firefighters.

Long-term psychological effects of exposure to a dangerous chemical were evaluated in a sample of firefighters who fought a large polyvinyl chloride (PVC) fire. When compared with nonexposed firefighter controls (n = 22), the exposed firefighters (n = 64) had significantly higher levels of demoralization and specific emotional distress 22 months after the incident. Longitudinal analyses of a subsample of exposed firefighter subjects (n = 55) surveyed 5 to 6 weeks after the fire and again 22 months later revealed that there was no reduction in symptomatology over time. Some psychological distress scores actually rose significantly between time points. Distress scores were also significantly correlated between time points. These results have a number of intervention and public health implications.

Psychological response of firefighters to a chemical fire.

Samples of firefighter subjects (n = 80) and a comparison group (n = 15) were contrasted on a number of postincident psychological distress measures in the aftermath of a polyvinyl chloride (PVC) fire. Using a structured, self-administered questionnaire, firefighter subjects were found to be more psychologically distressed on demoralization, specific emotional distress, and perceived threat to physical health. After controlling for baseline characteristics on which subjects and the comparison group differed, these between-group effects remained significant. The three outcome scales, while correlated, measure different components of psychological distress.

Across-shift changes in the pulmonary function of meat-wrappers and other workers in the retail food industry.

Pulmonary function was measured before, during, and after the end of the workshift in 83 workers in the retail food industry. All acute changes in forced expiratory volume in 1 s were standardized for lung size before the magnitude of the changes were compared between the workers exposed and unexposed to the use of hot wires for cutting plastic film. No association was found between acute drop in pulmonary function and either direct or indirect exposure in the absence of a history of asthma or allergy to inhaled materials. The borderline significance of an interaction term between exposure and asthma/allergy in a regression analysis suggests that workers with a history of asthma or atopy may have an acute response to hot-wire wrapping emissions.

Carcinogenicity and epidemiological profile analysis of vinyl chloride and polyvinyl chloride.

The carcinogenicity of vinyl chloride and polyvinyl chloride (VC/PVC) is reviewed with specific attention to the gaps in knowledge for risk estimation and epidemiological presentation of the available data. Although experimental studies have demonstrated the carcinogenicity and mutagenicity of VC/PVC in general, the epidemiologic studies available for review do not include an assessment of carcinogenic risk among humans exposed to these chemicals. This conclusion is based on the observation that the majority of cohort studies reviewed lacked sufficient statistical power because of small sample sizes. Further, in epidemiological studies, individuals were not followed over an adequate period of time during which cancer could become clinically manifest.

Occupational hazards in the VC-PVC industry.

Overall, the results of the analysis of 12 studies of VC production and polymerization workers demonstrate an enormously elevated risk of liver malignancies, the possibility of a twofold increased risk of brain and central nervous system tumors and perhaps, also, of malignancies of the lymphatic and hematopoietic system. However, the role of other agents cannot be excluded in the etiology of nonhepatic malignancies. Bronchogenic carcinoma does not appear to be increased from exposures to VC monomer, although a relationship to PVC dust was suggested in one study. These conclusions must be considered in light of limited data on workers followed more than 25 years from onset of exposure. Considering the numbers of observed and expected deaths in all studies, it would appear that the excess of malignancies at nonhepatic sites is less than the excess of liver tumors. Data presented elsewhere in this volume (Nicholson and Henneberger, 1983) suggest that exposure reductions in 1974 may have virtually eliminated the VC-associated risk of liver cancer if the current U.S. standard is met. To the extent that VC exposure is associated with other cancers, a similar risk reduction would be expected. Raynaud's phenomenon, acroosteolysis, scleroderma-like skin lesions, hepato- and splenomegaly with noncirrhotic hepatic fibrosis, and severe portal hypertension have been associated with past heavy exposures to VC. Evidence exists that the liver disease and portal hypertension may progress following cessation of exposure. However, all of the above syndromes were found largely in heavily exposed individuals. Their occurrence would be much less likely in workers exposed only to concentrations currently allowed. Pulmonary deficits, X-ray abnormalities, and, perhaps, lung cancer have been associated with VC/PVC exposure. Because of the possible contribution of PVC dust to these findings, engineering controls during polymer drying, bagging and usage are warranted.

[Toxic and metabolic liver injury (author's transl)]. / Toxische Leberschäden.

Water soluble exogenous compounds are commonly excreted by the kidneys, but most of the exogenous substances are lipid soluble and have therefore first to be metabolized in the liver to water soluble compounds. Depending upon the nature of the chemical compound, the metabolism in the liver leads either to detoxification or toxification. Alcohol belongs to the most important substances which may cause severe liver injury. Alterations of the liver due to hydrocarbons as well as carcinogens, mycotoxins and thorium dioxide are relatively rare. Compounds such as analgesic and antiarrhythmic drugs, antibiotics, oral antidiabetic agents, antihypertensive and antirheumatic agents, chemotherapeutic drugs, hormones, laxatives, psychotropic drugs, thyreostatic and antineoplastic agents may also cause liver injury. For establishing the diagnosis, a detailed past history is required especially with respect to alcohol and drug consumption as well as regarding occupational exposure towards toxic compounds. Although the determination of liver enzyme activities in the serum may give some indication for liver cell injury, the histological examination of the liver by needle biopsy is required for the diagnosis. The therapy consists of the exclusion of the toxic compound and, if possible, of an increased elimination of the ingested toxins.

[Prevention in general practice: what is dangerous for liver cells?]. / Vorsorge in der Praxis: Was ist schädlich für die Leber?

The liver is engaged in detoxication and elimination of toxic-nutritional foreign material. In addition it is of high affinity to viruses and parasites. Different influences may cause pathological reactions, which are of great consequence to the normal and even more to the previously damaged liver. In general, interactions and cumulative effects of different toxic agents occur. The increase of chronic hepatic disorders in the last years has to be noticed considering economic and social medical aspects. At the first place of agents with a toxic effect to the liver there is alcohol, followed by hyperalimentation and malnutrition. Numerous drugs with different reactions to liver morphology, liver impairment caused by environmental influences and infections retain further places. Prophylaxis and therapy of toxic-nutritional liver damage is based on recognition and elimination of the noxes. Patients with chronic liver disease need a special management and consultation by their physician.