John H. Lange

Epidemiologic evidence of cancer risk in textile industry workers: a review and update.

A meta-analysis of epidemiologic studies for textile industry workers was undertaken in an attempt to evaluate whether the cancer risk varies within the textile industry in relation to the job held or the textile fiber used. We combined studies published up until 1990, when an ad hoc IARC Monograph was issued, and those published after 1990 with the aim of appreciating evidence of reversing trends in cancer risk. Observed and expected cases reported in the original studies were summed up and the totals were divided to obtain a pooled relative risk (PRR) with a 95% confidence interval (CI) estimated with a fixed-effect model. We calculated a chi-square test (x2) of heterogeneity among studies. When PRR and x2 were both significant, PRR and CI were calculated with a random-effect model and the source of heterogeneity was investigated. Lung cancer risk was around 0.4 in the first study on cotton workers published in 1936, around 0.7 in subsequent studies, mostly published in the 1970s and 1980s, and around 1.0 in the last studies published in the 1990s. Papers published in the 1970s and 1980s produced consistent risk estimates for lung cancer risk, which was significantly lower than 1.0 in workers exposed to cotton (PRR 3/4-0.77; CI3/4-0.69-0.86) and wool dust (0.71; 0.50-0.92), as well as in carders and fiber preparers (0.73; 0.54-0.91), weavers (0.71; 0.56-0.85), and spinners and weavers (0.78; 0.66-0.91). Lung cancer PRRs did not significantly deviate from 1.0 in textile workers using synthetic fibers or silk, and in dyers. Increased PRRs were found for sinonasal cancer in workers exposed to cotton dust, and in workers involved in spinning or weaving (4.14; 1.80-6.49). PRR was 1.46 (1.10-1.82) for cancer of the digestive system in textile workers using synthetic fibers or silk, and 1.34 (1.10-1.59) for colorectal cancer in spinners and weavers. The increased bladder cancer PRR in dyers (1.39; 1.07-1.71) is generally attributed to textile dye exposure. In studies published after 1990, there is a general tendency to move toward unity for all the cancer risk estimates, leading to an increasing heterogeneity among studies. Since adjustment for smoking made little difference to the findings, the latter could be attributed to the exposure to textile dusts. The recent findings could be due to a lowering of dust concentration in the workplaces. The reduction of cases of upper respiratory tract cancer parallels with a corresponding increase of lung cancer cases. So, preventive measures have paradoxically increased the lung cancer burden to the textile workers.

Feasibility of a screening programme for lung cancer in former asbestos workers

BACKGROUND Low-dose computed tomography (CT) has been found to detect more Stage IA lung cancer than chest x-ray. AIMS To investigate whether lung cancer screening with CT was effective and acceptable in former asbestos workers. METHODS CT scanning was carried out following the protocol previously described in the literature. A questionnaire was used to assess cumulative asbestos exposure. An economic analysis was also performed. Informed consent was obtained from all patients. RESULTS A total of 1119 male asbestos workers (58% of invited) were examined, of whom 65% were smokers or ex-smokers. Mean age was 57.1 years with mean cumulative exposure to asbestos of 123 fibres/ml x years. Pleural plaques were found in 375 workers (32%), while 338 workers (29%) were included in the radiological follow-up, which led to 25 biopsies (13 of lung, 9 of pleura, 3 of both) and five screen-detected lung cancers (0.4%), one in Stage I. Incidence rate was 149 per 10(5), equal to that in the male general population of similar age. The expenses for diagnosis were 1014 and 244962 Euro per screened subject and screen-detected lung cancer case, respectively. CONCLUSIONS Screening adherence and frequency of detection were low, while costs and radiation dose were high. In spite of a high cumulative asbestos exposure, lung cancer risk was not increased relative to the general population. The screening programme was not felt to be cost-effective from the perspective of the government as a third-party funding agency.

Osteopontin, asbestos exposure and pleural plaques: a cross-sectional study

BackgroundOsteopontin (OPN) is a plasma protein/cytokine produced in excess in several malignancies. In a recent study OPN was reported as being related to the duration of asbestos exposure and presence of benign asbestos-related diseases; however, it was unclear whether this protein was an indicator of exposure or effect.MethodsIn 193 workers, 50 with pleural plaques (PP), in whom different indicators of past asbestos exposure were estimated, OPN plasma levels were assessed using commercial quantitative sandwich enzyme immunoassays according to the manufacturers instructions.ResultsOsteopontin increased with increasing age and several aspects of asbestos exposure, without differences related to the presence of pleural plaques. At multivariable regression analysis, the explanatory variables with a significant independent influence on OPN were length of exposure (positive correlation) and time elapsed since last exposure (positive correlation).ConclusionsSince asbestos in lung tissue tends to wane over time, OPN should decrease (rather than increase) with time since last exposure. Therefore, OPN cannot be a reliable biomarker of exposure nor effect (presence of pleural plaques).

How do you interpret regulations: through science or agency rules?

Sir ¡/ Wallingford and Snyder (2001) suggest that asbestos exposures for those performing cleanup at the World Trade Center (WTC) disaster were below the Occupational and Safety Administration (OSHA) permissible exposure limit (PEL) of 0.1 f/ cc-TWA and bulk asbestos sample concentrations do not represent a health hazard. Samples above the PEL, as determined by phase contrast microscopy (PCM), were reanalyzed using transmission electron microscopy or a modified (differential) polarized light microscopy. The authors’ reported that three bulk asbestos samples had a concentration greater than 1%, which is the US Environmental Protection Agency’s definition of asbestoscontaining material (ACM). The asbestos concentrations reported by Wallingford and Snyder ranged between 1 and 3%. The authors’ suggest that there is no occupational hazard at the WTC from asbestos. Other studies (Ilgren, 2001; Lange, 2001; 2003) on the WTC have reported higher exposure levels (including bulk samples), which were also more widely distributed around the site. This indicates that there is some discrepancy in the observed asbestos concentrations. Regulatory agencies do not examine asbestos exposure from a scientific perspective, but rather from the strict interpretation of standards (Lange, 2001). This has become know as legislating science (Lange, 2003). However, when these agencies evaluate exposure of others, which is mainly private parties, their interpretation of regulations is as strictly written, although for themselves the interpretation is based on economics, practicability, and reasonableness (Jenkins, 2001; Lange, 2003; 2003a). This has resulted in two different regulatory schemes ¡/ one for regulating agencies and the other for those they regulate. Regulatory agencies frequently cite private parties for violating asbestos standards when the material in question was Í/1% but B/5% asbestos (Lange, 2003). Why 1% was selected as the standard for defining ACM is apparently not based on health standards but opinion (Lange, 2003). These agencies have also issued citations for violation of the OSHA PEL ¡/ invoking the one-strike principle (Lange, 2003). OSHA’s asbestos standard specify using PCM for determining airborne concentrations of asbestos and does not list or identify any other method or procedure. As suggested by Wallingford and Snyder, as well as on the OSHA website, in order to lower the exposure limit at the WTC, a modified PCM method was employed. Certainly, this questions as to whether there is intent by regulatory agencies to change the methodology for determining exposure levels (Lange, 2003). This paper does not mention the myriad of health problems that are emerging as a result of the WTC disaster (Lange, 2003b). Although these problems are unlikely directly related to asbestos exposure, it is suggested that this agent contributed to the mixture effect that is likely the cause of observed health problems. I would even suggest that the number of lives lost in this tragedy would be less than that which will be lost to chronic problems from the subsequent exposure. Modification of agency methods demonstrates (Lange, 2003) the inadequacy of some environmental and occupational agencies in regulating themselves. Regulatory agencies need to begin looking at standards from a health-based set of glasses and not through legislating of science. Many environmental regulations now exist for convenience and maintenance of the bureaucracy of those agencies enforcing the standards and not for public health protection (Jenkins, 2001; Lange, 2003). Regulations also need to be examined from a practical point of view. The issues raised by Wallingford and Snyder are important and strive for practicality of Toxicology and Industrial Health 2002; 18: 107¡/108

Airborne exposure and soil levels associated with lead abatement of a steel tank

This study reports on airborne exposure levels and soil concentrations of lead in regard to abatement of a steel structure (water tank). The tank was de-leaded by abrasive sand blasting. The ball of the tank had a lead surface level that exceeded the Environmental Protection Agency (EPA) definition of lead-based paint (LBP) (0.5% lead), but paint on stem and base was below this criterion. Personal and area airborne samples were collected during different activities of lead abatement of the tank. Summary results suggest during abrasive blasting of ball and stem/base personal exposure levels, as reported with arithmetic and geometric means, exceed the Occupational Safety and Health Administration (OSHA) permissible exposure limit (50 g/m3). Highest personal exposure (occupational exposure) was associated with blasting of ball. Distribution of airborne and soil samples suggest non-normality and is best represented by a logarithmic form. Geometric standard deviations for air and soil lead support a non-normal distribution. Outlying values were found for personal and area air samples. Exposure levels associated with blasting stem/base section of tank support OSHA’s policy requiring air monitoring of work at levels below the criterion established by EPA in identifying LBP. Area samples were statistically lower than personal samples associated with blasting ball and stem/base of tank. Exposure data suggest that workers performing abatement on steel structures have elevated lead exposure from surface lead. Respirator protection requirements are discussed. Soil lead concentration was suggested to decrease as distance increased from tank. Soil lead is suggested to be a result of deposition from LBP on tank surface. Minimal efforts were required to reduce average lead soil levels below EPA’s upper acceptable criterion (1200 ppm Pb).