Toxicology and Industrial Health

The goal of sustainable use is indefinite use of the planet by humankind. This objective, in turn, requires that the planet’s ecological life support system, consisting of natural capital and ecosystem services, remains healthy for an indefinite period. Achieving sustainability will require a new view of the responsibilities of professionals, such as ecotoxicologists, to ensure a healthy ecological life support system. Because both human society and natural systems are complex and multivariate, a high degree of uncertainty will remain. Therefore, sound judgment will be needed in determining what, if any, precautionary measures should be taken until more robust information has been gathered.

The role of ecotoxicologists in the quest for sustainable use of the planet is quite varied: 1) shifting goals and endpoints from an absence of harm to persuasive evidence of health; 2) increasing both temporal and spatial scales of ecotoxicological studies; 3) achieving a critical mass of qualified personnel; 4) including demographic change in ecotoxicological analysis and judgment; 5) developing new ecological thresholds; 6) being prepared for environmental surprises; 7) focusing on design for a quality environment; 8) developing ecosystem services as endpoints in ecotoxicological studies, and 9) being prepared for climate change and other events that might destabilize the biosphere and require major adjustments in the process of ecotoxicological testing. Both sustainable use of the planet and the field of ecotoxicology are rapidly developing fields that are mostly evolving in isolation from each other. To be successful, they must co-evolve.

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.

Suspended particulate concentrations were measured at the Tzu Yun Yen temple in the Taichung region of Taiwan. The temple performs traditional incense burning. A universal sampler and a micro-orifice uniform deposited impactor (MOUDI) sampler with a dry deposition plate were used to measure the particulate concentrations. The results show that the average PM_2.5/PM₁₀ ratio was 74% during the incense burning period at this temple. In addition, the average suspended particulate (PM₁₀) element concentration of anthropogenic element Zn (495 ng/m³) was higher than the other anthropogenic elements (Pb, Mn, Ni, and Cd). Furthermore, the average mass size distribution was bimodal with major peaks occurring at 0.32-0.56 mm and 5.6-10 mm during the incense burning period. The dry deposition velocities of Cd used fine particulates (PM_2.5) and suspended particulate (PM₁₀) mode were 1.86 and 0.99 cm/s in this study, respectively.

3,3?-dichlorobenzidine (DCB) can be metabolically N-acetylated and/or N-oxidized, and can form hemoglobin adducts. Gas chromatography/mass spectrometry-selected ion monitoring detection mode (GC/MS-SIM) could be a good analytical method to detect them. 4-Aminobiphenyl and phenanthrene-d₁₀ were used as internal standards, and standard metabolites of DCB were synthesized from DCB. Pyridine is a promoter and acetic acid is a controller in the acetylation of DCB during titrating with acetyl chloride. After washing with acetone, the purity of N-acetyl DCB and N, N?-diacetyl DCB were 98.72% and 98.82%, respectively.

The maximum detection limits (MDLs) by GC/MS-SIM were 0.5 mg/L in DNA adduct and 1.0 ng/g in hemoglobin for DCB and N-acetyl DCB. The base peaks of their fragmentation pattern were 252 m/z at the peak of DCB, 252 m/z and 294 m/z at the peak of N-acetyl DCB, and 252 m/z, 294 m/z, and 336 m/z at the peak of N, N?-diacetyl DCB. This analytical method was applied to determine hemoglobin adducts formed in young female Sprague -Dawley rats orally exposed with 20, 30, and 40 mg DCB/kg/day for three weeks. Two adducts were detectable by GC/MS-SIM after alkaline hydrolysis of hemoglobin samples and extraction. The structure of these adducts could be assigned to DCB and N-acetyl DCB by co-chromatography with the synthetic standards.

After the first week of treatment, the total amount of hemoglobin adducts determined was 837.5∼2501 ng/g hemoglobin. The adduct levels were increased up to 1203.3∼2605.4 ng/g after the second week, and slightly decreased after the third week. The ratio of DCB and N-acetyl DCB was nearly similar in all treatment groups at the third week, such as 4.28∼4.78. Three different treatments (20, 30, and 40 mg DCB/kg) of rats resulted in dose-proportional increases in the total and DCB amount of hemoglobin adducted formed for three weeks. The relative contribution of DCB and N-acetyl DCB to the total hemoglobin adduct level was strongly dose dependent. The results show that GC/MS-SIM is suitable for the biological monitoring of humans exposed to DCB or DCB-containing products

Acute paraquat poisoning is often fatal. Many studies have investigated successful treatment modalities, but no standard treatment yet exists. The purpose of this study was to determine the predictors of survival after acute paraquat poisoning in 602 patients. The paraquat exposure was assessed based on the amount of ingested paraquat and a semiquantitative measure of the urine level of paraquat. Initial clinical parameters including vital signs, hemoglobin, white-blood-cell count, pH, PaCO₂, PaO₂, blood urea nitrogen, creatinine, aspartate aminotransferase, alanine aminotransferase, total bilirubin, amylase, and glucose were obtained at the time of arrival at the emergency room. Outcomes after acute paraquat poisoning were categorized as survivors and nonsurvivors. Multiple logistic regression analysis was applied to assess the predictors of survival after acute paraquat poisoning.

Some patients (55.5%) survived after oral ingestion of paraquat, whereas all those exposed to paraquat percutaneous or inhalational route survived. The amount of paraquat (24.5% concentrate of 1,1′-dimethyl-4,4′-bipyridium dichloride) ingested was 45.69 ^/ 74.1 mL (mean9 ^/ SD). In addition to degree of paraquat exposure, survival after acute paraquat poisoning was associated with age, respiratory rate, pH, PaCO₂, hemoglobin, white-blood-cell count, blood urea nitrogen, amylase, and the number of failed organs in multiple logistic regression analysis. In conclusion, young age, percutaneous or inhalational route, exposure to less paraquat, and lesser degrees of leukocytosis, acidosis, and renal, hepatic, and pancreatic failures on admission are good prognostic factors of survival after acute paraquat poisoning.