Giovanni Carelli

Effects of Occupational Trichloroethylene Exposure on Cytokine Levels in Workers

Objective: We sought to investigate trichloroethylene-induced alterations of the immune system in humans. Methods: The levels of interleukin-2, interleukin-4, and interferon-&ggr; in sera obtained from workers exposed to trichloroethylene were determined and compared with those of internal and external control subjects. Results: In workers with a mean urinary trichloroacetic acid concentration of 13.3 ± 5.9 mg/g creatinine, exposed to a mean environmental trichloroethylene level of 35 ± 14 mg/m3, we observed a significant increase in sera interleukin-2 and interferon-&ggr; levels and a reduction in interleukin-4 concentrations compared with those of workers from the internal and external control groups. Conclusions: This study provides the first report on quantitative immune changes induced by occupational exposure to low levels of trichloroethylene and strongly suggests that exposure to this substance alters immunohomeostasis in humans with possible effects on health.

Exposure of rome city tram drivers to airborne platinum, rhodium, and palladium

Objective: To investigate the exposure of tram drivers of Rome to Pt, Rh, and Pd in total suspended particulate, PM10, and PM2.5 fractions. Methods: Sampling was performed on a tram running on about 15-km pathway characterized by a medium-high traffic car density. The analytical determination of metals was performed using inductively coupled plasma mass spectrometry. Results: Mean element values (in pg/m3) total suspended particulate, PM10, and PM2.5, were Pt, 20.3, 14.1, and 8.86, Rh, 3.99, 2.83, and 1.94, and Pd, 82.1, 58.0, and 15.2, respectively. Conclusions: Although the Pt, Rh and Pd levels in urban air were found to be still 8 to 11 orders of magnitude below the values thought to cause adverse effects on adult worker health, periodic environmental monitoring would be necessary to detect possible increments which could affect occupational exposure of tram drivers.

Evaluation of occupational exposure to n-nitrosamines in a rubber-manufacturing industry

Objective: We sought to determine volatile N-nitrosamines levels in the air of a rubber-manufacturing industry and to measure urinary N-nitrosamines concentrations in exposed workers. Methods: Personal monitoring of 34 workers was performed by sampling nine airborne N-nitrosamines in four factories that manufactured rubber drive belts for automotive engines. Urinary N-nitrosamine levels were determined in all workers and in a control group of 26 subjects. Analyses were conducted by capillary gaschromatography–thermal energy analyzer. Results: Airborne and urinary N-nitrosamines levels were very low and, in most cases, below the limit of detection (0.06 &mgr;g/m3 and 0.1 &mgr;g/L, respectively). Conclusions: Although airborne and urinary N-nitrosamines levels were found to be very low, exposed workers should still be monitored constantly because some of these substances are known to be genotoxic and carcinogenic.

Lead-related effects on rat fibroblasts.

Lead (Pb) is an environmental toxicant that can induce structural and functional abnormalities of multiple organ systems, including the central nervous and the immune systems. The aim of this study was to evaluate the effects of extracellular Pb supplementation on the cellular content of the metal and on the proliferation and the survival of normal rat fibroblasts.We found that the concentration of Pb in the culture medium was 0.060 μM and the normal Pb concentration in rat fibroblasts was 3.1 ± 0.1 ng/107 cells. Then we exposed the cells to increasing concentration of Pb (as Pb acetate) from 0.078–320 μM. We observed a dose‐dependent inhibition of cell proliferation after 48 h, which was already apparent at a concentration of 0.312 μM (p = 0.122) and became statistically significant for concentration higher than 0.625 μM (p = 0.0003 at 5 μM). Cell proliferation was completely compromised at 320 μM Pb total inhibition of cell proliferation.To investigate the mechanisms of Pb‐mediated inhibition of cell proliferation, we evaluated the occurrence of apoptosis in the same cells and found that cytosolic DNA fragments, hallmark of apoptotic cell death, increased significantly at Pb concentrations from 2.5–10.0 μM. The occurrence of apoptosis was also confirmed by FACS analysis which showed the appearance of a subdiploid peak at Pb concentrations from 5–20 μM. The distribution of cells in the cell cycle showed a dose‐dependent accumulation of cells in the G0/G1 phase mainly compensated by a decrease in the percentage of cells in the S phase. In conclusion, our results demonstrate that induction of apoptosis contributes to the Pb‐induced inhibition of cell proliferation in rat fibroblasts.

Exposure evaluation to airborne polycyclic aromatic hydrocarbons in an italian airport.

The aim of this study was to use environmental monitoring to evaluate occupational exposure to polycyclic aromatic hydrocarbons (PAHs) and biphenyl in an Italian airport. Air was sampled using a quartz fiber filter, a polyurethane foam, and an XAD-2 layer. After extraction with dichloromethane, concentration and purification analyses of 25 PAHs (including biphenyl) were carried out by gas chromatography-ion trap mass spectrometry. In winter 2005, 12 air samples were taken at 120 L/min for 24 hours in three different areas of the airport. PAH levels were found to be generally low. In all investigated areas, the higher levels refer to naphthalene (130–13,050 ng/m3), 2-methylnaphthalene (64–28,500 ng/m3), 1-methylnaphtalene (24–35,300 ng/m3), and biphenyl (24–1610 ng/m3). However, in some instances, for compounds such as benzo[b+j+k]fluoranthene and benzo[a]pyrene, two high-boiling PAHs, the levels found (54.2 ng/ m3 and 8.6 ng/m3, respectively) can be considered of some concern.

Interference effect in the atomic absorption spectrometric determination of arsenic in filter-collected air samples

Abstract The arsenic response obtained by arsine generation is decreased by the presence of the filter digest; a period of 25 min after mixing is needed before added arsenic gives a constant response.

Contribution of Dental Amalgam to Urinary Mercury Excretion in Children

Woods et al. (2007) studied a group of children (n = 507) who were exposed by inhalation to elemental mercury (Hg0) from dental amalgam fillings. In the study, 253 subjects were exposed, whereas the remaining 254 children, the control group, were exposed to composite resin. We consider the experimental design of their study to be adequate, but we do have questions about their methods of data handling and interpretation. For example, we do not understand why instead of always using creatinine-adjusted Hg levels, they used—in some instances—unadjusted Hg levels. In fact, there is continuous alternation and exchange between the two biological concepts (i.e., between the unadjusted and the adjusted concentrations). There are at least three well-grounded and well-known reasons that creatinine adjustment is essential: a) urinary creatinine accounts for variations in 24-hr excretion (Aito et al. 1983); b) urinary creatinine adjustment reportedly reflects Hg blood levels (Smith et al. 1970) and possibly Hg body burden; and c) in the light of established knowledge, Hg blood levels reflect recent exposure (Piotrowski et al. 1975). Accordingly, the lack of significance between the Hg levels (not adjusted for creatinine) of the amalgam and the control subgroups at year 7, the final year of the study by Woods et al. (2007), is probably a bias that is indicated by the disappearance of overlapping if creatinine adjustment had been performed, as suggested by Aitio et al. (1983) as long as 25 years ago. Also, because no adjusted data were reported for male and female levels, the impact of such an adjustment cannot be conjectured by the reader. Subsequently this prevents accurate evaluation of the Hg level trend over the years. It should be pointed out that the data of Woods et al. (2007) do not allow us to extrapolate whether or not the exposed subgroup is in the steady state, because this condition depends on the time lag between urine collection and the last amalgam treatment(s). This limitation prevents an accurate interpretation of the decrease in urinary Hg levels over years. Geller (1976) reported that Hg sulfide can coat Hg0, thereby slowing down the release of Hg vapor. Although no specific study has determined whether this is true for amalgams, we cannot exclude that Hg oxidation may yield Hg sulfide on the amalgam surface. Woods et al. (2007) speculated about the decrease in Hg urinary excretion over years, but they did not consider the possibility of sulfide formation. Moreover, they did not explain the decrease in Hg levels over time after year 2 but simply stated that “the rate of urinary [Hg] excretion exceeds the rate of [Hg] exposure from dental amalgam.” The formation of a thin film of Hg sulfide on amalgam surfaces could be an explanation, especially since the Hg body burden—and consequently Hg urinary levels—may be either in the steady state or at an increasing elimination rate because of the addition of new fillings. Furthermore, we feel that the use of the term “dose–effect relationship” by Woods et al. (2007) is questionable. Also, it is not clear if the term “dose” refers to the number of additional amalgam fillings over the years or to the difference between means. Also, “effect” has a completely different meaning in toxicology. In this case, another term should be used to more accurately indicate the difference in two urinary Hg levels. In our opinion, “differential dose minus follow-up years” would be more appropriate in the text than “dose effect.” Woods et al. (2007) stated that in children who received “up to 9 initial amalgam fillings, urinary Hg returned to pre-treatment value within one year,” but this statement is not clear because this trend applies only to children who received 0–4 amalgam fillings at baseline but not to the group that received 5–9 [Figure 4; Woods et al. (2007)]. Finally, Woods et al. (2007) omitted error bars from their Figure 4; SE or SD could have been easily calculated by the theory of error propagation and would probably have addressed the discussion more accurately, or at least would have tempered some conclusions, especially with regard to confirmation of the “whole-body biological half-time of Hg on the order of 60–70 days.” This half-time is correct but there is a large margin of uncertainty based on the experimental data. In conclusion, although Woods et al. (2007) used a well-structured experimental design, their conclusions are not accurate because of their handling of the experimental results and their use of basic toxicology terminology.

DOSE-RESPONSE RELATIONSHIPS IN HUMAN EXPERIMENTAL EXPOSURE TO SOLVENTS

Previous studies carried out in the field of experimental toxicology have shown evidence of biphasic dose-response relationships for different experimental models, end-points and chemicals tested. As these studies excluded humans as the experimental model, we have examined the literature of the last three decades in order to verify data concerning human experimental exposure with the aim of highlighting possible biphasic dose-response relationships. The substances used for experimental exposures included hydrocarbons, esters, alcohols, ketones, ethers, glycoethers, halogenated hydrocarbons, and carbon sulphide; the absorption route was inhalation. We did not detect any biphasic dose-response relationship and, in the studies reviewed, our examination revealed major methodological limitations that prevented us making a more detailed examination of experimental data. We concluded that the experimental data available did not allow us to support evidence of biphasic dose-response relationships in human experimental exposure to the above-mentioned chemical substances.

Hormesis and industrial hygiene: a new hypothesis for low-dose response in occupational risk assessment

The study of Jayjock and Lewis, `Implication of Hormesis for Industrial Hygiene’, represents a challenge for the scientific community to consider hormesis as a possible working hypothesis for redefining risk assessment strategy for low-dose exposures in the realm of industrial hygiene. This invited commentary aims at examining some aspects of the study for which no proven and conclusive scientific evidence has yet been found, such as the limited nature of some statistical tests, the calculation of the safety factor, the place occupied by hormesis in industrial hygiene and, finally, the impact that scarce knowledge of this phenomenon and rejection by part of the scientific community has on the possibility of using hormesis in the safeguarding of workers’ health.