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- Axmon, Anna, et al.
(author)
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Estimations of past male and female serum concentrations of biomarkers of persistent organochlorine pollutants and their impact on fecundability estimates.
- 2006
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In: Environmental Research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 101:3, s. 387-394
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Journal article (peer-reviewed)abstract
- Persistent organochlorine pollutants (POPs) have been suggested to have negative effects on a number of hormonal systems. Several studies performed retrospectively have reported a possible association between POP exposure and fertility, measured as time to pregnancy (TTP). However, these studies lack biomarkers of exposure at the time when the women tried to conceive. It has previously been found that past female serum concentrations of 2,2,4,4',5.5'-hexachlorobiphenyl (CB-153) can be estimated using a complex decay model, assuming that the biological half-life is 5 years, the yearly environmental reduction of the compound has been 3% since 1976, and the reduction of body burden due to lactation is 20% for periods up to 6 months and 30% for periods exceeding 6 months. In the present study, it is established that the model is valid also for estimations of past male serum concentrations of CB-153. Furthermore, the complex decay model was found to be useful also for estimating past serum concentrations of 1,1-dichloro-2,2-bis (p-chlorophenyl)ethylene (p,p'-DDE), assuming that the biological half-life of the compound is 8 years, the yearly reduction between 1971 and 1981 was 20% and after that 9%, and the reduction of body burden due to lactation is the same as that for CB-153. However, even though the estimated past serum concentrations of CB-153 and p,p'-DDE were found to be better proxy measures of actual past concentrations than current serum concentrations, there was little change in the rank order of the population investigated. Thus, the effect estimate for TTP was similar for both proxy measures when using categorized measures of exposure. (c) 2005 Elsevier Inc. All rights reserved.
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- Barregård, Lars, 1948, et al.
(author)
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Leukaemia incidence in people living close to an oil refinery.
- 2009
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In: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 109:8, s. 985-90
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Journal article (peer-reviewed)abstract
- OBJECTIVES: To assess the incidence of leukaemia in an area downwind of a large oil refinery emitting carcinogenic volatile organic compounds (VOCs) including benzene. METHODS: Using a dispersion model and the prevailing wind direction, two parishes with about 5000 inhabitants were a priori considered to be exposed to VOCs from the refinery. Numbers of observed and expected leukaemia cases in 1975-2004 were calculated using regional sex- and age-specific incidence rates. In addition, five nearby parishes (12000 inhabitants), considered unaffected by the emissions, served as a local reference area. Based on emission data, dispersion modelling and VOC measurements, the refinery's contribution to the population's exposure to carcinogenic VOCs was estimated. Published "unit risks" for carcinogenic VOCs were used to estimate the expected excess leukaemia risk. RESULTS: The incidence of leukaemia in the "exposed parishes" was significantly increased in 1975-2004 (33 cases v. 22 expected cases), owing to an increase in the last 10-year period, from 1995 to 2004 (19 cases v. 8.5 expected cases). The leukaemia incidence in the local control area was normal (50 cases v. 56 expected cases). The estimated contribution from the refinery to VOC concentrations was, however, only about 2 microg/m(3) (yearly average) for benzene, 2 microg/m(3) for ethylene, 0.5 microg/m(3) for 1,3-butadiene and 5 microg/m(3) for propene. Calculations of expected excess risk using published risk estimates would indicate a much lower excess risk in the exposed parishes. CONCLUSIONS: Using risk estimates extrapolated from high-level exposure, we would not expect an increase of leukaemia at low exposure to VOC emissions. Nevertheless, the clear elevation of leukaemia in the priori selected, exposed parishes was remarkable. Our finding may reflect a causal association due to emissions, but it could also be due to unknown confounding, or chance.
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- Belpomme, D., et al.
(author)
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The multitude and diversity of environmental carcinogens
- 2007
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In: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 105:3, s. 414-429
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Journal article (peer-reviewed)abstract
- We have recently proposed that lifestyle-related factors, screening and aging cannot fully account for the present overall growing incidence of cancer. In order to propose the concept that in addition to lifestyle related factors, exogenous environmental factors may play a more important role in carcinogenesis than it is expected, and may therefore account for the growing incidence of cancer, we overview herein environmental factors, rated as certainly or potentially carcinogenic by the International Agency for Research on Cancer (IARC). We thus analyze the carcinogenic effect of microorganisms (including viruses), radiations (including radioactivity, UV and pulsed electromagnetic fields) and xenochemicals. Chemicals related to environmental pollution appear to be of critical importance, since they can induce occupational cancers as well as other cancers. Of major concerns are: outdoor air pollution by carbon particles associated with polycyclic aromatic hydrocarbons; indoor air pollution by environmental tobacco smoke, formaldehyde and volatile organic compounds such as benzene and 1,3 butadiene, which may particularly affect children, and food pollution by food additives and by carcinogenic contaminants such as nitrates, pesticides, dioxins and other organochlorines. In addition, carcinogenic metals and metalloids, pharmaceutical medicines and cosmetics may be involved. Although the risk fraction attributable to environmental factors is still unknown, this long list of carcinogenic and especially mutagenic factors supports our working hypothesis according to which numerous cancers may in fact be caused by the recent modification of our environment. (C) 2007 Elsevier Inc. All rights reserved.
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6. |
- Berglund, Åsa, 1978-, et al.
(author)
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Oxidative stress in pied flycatcher (Ficedula hypoleuca) nestlings from metal contaminated environments in northern Sweden.
- 2007
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In: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 105:3, s. 330-339
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Journal article (peer-reviewed)abstract
- Metals have been shown to induce oxidative stress in animals. One of the most metal polluted terrestrial environments in Sweden is the surroundings of a sulfide ore smelter plant located in the northern part of the country. Pied flycatcher nestlings (Ficedula hypoleuca) that grew up close to the industry had accumulated amounts of arsenic, cadmium, mercury, lead, iron and zinc in their liver tissue. The aim of this study was to investigate if pied flycatcher nestlings in the pollution gradient of the industry were affected by oxidative stress using antioxidant molecules and enzyme activities. The antioxidant assays were also evaluated in search for useful biomarkers in pied flycatchers. This study indicated that nestlings in metal contaminated areas showed signs of oxidative stress evidenced by up regulated hepatic antioxidant defense given as increased glutathione reductase (GR) and catalase (CAT) activities and slightly but not significantly elevated lipid peroxidation and glutathione-S-transferase (GST) activities. Stepwise linear regression indicated that lipid peroxidation and CAT activities were influenced mostly by iron, but iron and lead influenced the CAT activity to a higher degree. Positive relationships were found between GST and lead as well as GR activities and cadmium. We conclude that GR, CAT, GST activities and lipid peroxidation levels may function as useful biomarkers for oxidative stress in free-living pied flycatcher nestlings exposed to metal contaminated environments.
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- Chen, Xiao, et al.
(author)
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Changes in bone mineral density 10 years after marked reduction of cadmium exposure in a Chinese population.
- 2009
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In: Environmental research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 109:7, s. 874-9
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Journal article (peer-reviewed)abstract
- The main focus of this study was to evaluate the long-term effects of Cd on forearm bone mineral density after the cessation of the ingestion of Cd-polluted rice. A total of 458 persons (294 women, 164 men) from three Cd exposure areas (low, moderately, and heavy) participated in this study. Those living in the moderate and heavy exposure areas ceased ingesting Cd-polluted rice (0.51 and 3.7mg/kg, respectively) in 1996 (10 years prior to present analysis). The participants completed a questionnaire and bone mineral density (BMD) was measured by dual energy X-ray absorptiometry (DXA) at the proximal radius and ulna. The changes and change percentage in forearm bone density and the prevalence of osteoporosis between 1998 and 2006 were used as markers of bone recovery. The Cd concentrations in urine (UCd) and blood (BCd) in 1998 were used as Cd exposure markers. The values of the BMD change and change percentage of groups in which UCd was above 5microg/g creatinine (microg/g crea) and BCd was above 10microg/L were significantly higher than those of the low-exposure groups (in women, p<0.001; in men, p>0.05). The BMD change and change percentage correlated positively with the UCd and BCd (in women, p<0.01; in men, p>0.05). Analysis of the Z-score revealed that the prevalence of osteoporosis in 2006 was higher than that in 1998 and increased along with the level of UCd and BCd in both women and men, especially for those subjects with the higher BCd [BCd>5microg/L, OR=3.45 (0.95-13.6); BCd>10microg/L, OR=4.51(1.57-13.54)] and UCd [UCd>10microg/g crea, OR=4.74 (1.82-12.81)] in women. It is concluded that decreasing dietary cadmium exposure at the population level is not associated with bone recovery at the individual level, and the adverse bone effects of Cd exposure persisted after the main source of Cd exposure had been blocked, especially in women.
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- Engstrom, Annette, et al.
(author)
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Cadmium-induced bone effect is not mediated via low serum 1,25-dihydroxy vitamin D
- 2009
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In: Environmental Research. - : Elsevier BV. - 1096-0953 .- 0013-9351. ; 109:2, s. 188-192
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Journal article (peer-reviewed)abstract
- Cadmium is a widespread environmental pollutant, which is associated with increased risk of osteoporosis. It has been proposed that cadmium's toxic effect on bone is exerted via impaired activation of vitamin D, secondary to the kidney effects. To test this, we assessed the association of cadmium-induced bone and kidney effects with serum 1,25-dihydroxyvitamin D (1,25(OH)(2)D); measured by enzyme immunoassay. For the assessment, we selected 85 postmenopausal women, based on low (0.14-0.39 mu g/L) or high (0.66-2.1 mu g/L) urinary cadmium, within a cross-sectional population-based women's health survey in Southern Sweden. We also measured 25-hydroxy vitamin D. cadmium in blood, bone mineral density and several markers of bone remodeling and kidney effects. Although there were clear differences in both kidney and bone effect markers between women with low and high cadmium exposure, the 1,25(OH)(2)D concentrations were not significantly different (median, 111 pmol/L (5-95th percentile, 67-170 pmol/L) in low- and 125 pmol/L (66-200 pmol/L) in high-cadmium groups; p = 0.08). Also, there was no association between 1,25(OH)(2)D and markers of bone or kidney effects. It is concluded that the low levels of cadmium exposure present in the studied women, although high enough to be associated with lower bone mineral density and increased bone resorption, were not associated with lower serum concentrations of 1,25(OH)(2)D. Hence, decreased circulating levels of 1,25(OH)(2)D are unlikely to be the proposed link between cadmium-induced effects on kidney and bone. (C) 2008 Elsevier Inc. All rights reserved.
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10. |
- Frisk, Peter, et al.
(author)
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Tissue uptake of mercury is changed during the course of a common viral infection in mice
- 2008
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In: Environmental Research. - : Elsevier BV. - 0013-9351 .- 1096-0953. ; 106:2, s. 178-184
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Journal article (peer-reviewed)abstract
- Mercury (Hg) has been shown to have immunotoxic effects and to influence the severity of infection. However, the impact of infection on the normal Hg homeostasis in different target organs involved in the disease process has not been studied. In this study, Hg was measured through inductively coupled plasma-mass spectrometry (ICP-MS) in the intestine, serum, liver, and brain on days 3, 6, and 9 of coxsackievirus B3 (CVB3) infection in female Balb/c mice. The severity of the infection was assessed from clinical signs of disease and the number of virus particles in infected organs. CVB3 and gene expression of metallothionein 1 (MT1) was measured by reverse transcription-polymerase chain reaction (RT-PCR). Gene expression of MT1 increased and peaked on day 3 in the brain (93%, p<0.01) and liver (19-fold, p<0.01) and on day 6 in the intestine (seven-fold, p<0.01). This peak in MT1 in the liver and brain corresponded to the peak in virus numbers in these tissues. Hg in the intestine and serum tended to decrease on all days of infection. The maximum decrease, in comparison with non-infected mice, occurred in the intestine (78%, p<0.001) on day 9 and in serum (50%, p<0.05) on day 6. However, in the brain, Hg increased by 52% (p<0.05) on day 6. Hg went unchanged in the liver. An infection-induced increase of Hg in the brain but unchanged level in the liver may be due to the peak of virus replication and an associated infection-induced expression of MT1. Moreover, the decrease of Hg in serum and the intestine but a concomitant intestinal increase in MT1 on day 6 may reflect a flux and increased retention of Hg to infected organs such as the brain. The pathophysiological interpretation of these preliminary findings requires further research.
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