Arsenic

Maternal exposure to metals and time-to-pregnancy: The MIREC cohort study

Posted by

0


Abstract

Objective

To study the association between maternal exposure to arsenic, cadmium, lead, manganese and mercury, time-to-pregnancy (TTP) and infertility.

Design

Pregnancy-based retrospective TTP cohort study.

Setting

Hospitals and clinics from ten cities across Canada.

Population

A total of 1784 pregnant women.

Methods

Concentrations of arsenic, cadmium, lead, manganese and mercury were measured in maternal whole blood during the first trimester of pregnancy as a proxy of preconception exposure. Discrete-time Cox proportional hazards models generated fecundability odds ratios (FOR) for the association between metals and TTP. Logistic regression generated odds ratios (OR) for the association between metals and infertility. Models were adjusted for maternal age, pre-pregnancy body mass index, education, income, recruitment site and plasma lipids.

Main Outcome Measures

TTP was self-reported as the number of months of unprotected intercourse to become pregnant. Infertility was defined as TTP longer than 12 months.

Results

A total of 1784 women were eligible for the analysis. Mean ± SD maternal age and gestational age at interview were 32.2 ± 5.0 years, and 11.6 ± 1.6 weeks, respectively. Exposure to arsenic, cadmium, manganese or mercury was not associated with TTP or infertility. Increments of one standard deviation of lead concentrations resulted in a shorter TTP (adjusted FOR 1.09, 95% CI 1.02–1.16); however, the association was not linear when exposure was modelled in tertiles.

Conclusion

Blood concentrations of metals at typical levels of exposure among Canadian pregnant women were not associated with TTP or infertility. Further studies are needed to assess the role of lead, if any, on TTP.

1 INTRODUCTION

Environmental exposure to metals is a public health concern given their wide dispersion in the environment and potential endocrine disruptive properties.1–3 An endocrine endpoint of interest in reproductive and environmental epidemiology is human fecundity given the increased rates of gynaecological conditions associated with impaired fecundity and possible association with exposure to endocrine-disrupting chemicals.4–7 There is evidence linking metals like arsenic, cadmium, lead and mercury to impaired ovarian function through oxidative stress.1, 2 In contrast, other metals like manganese, an essential trace element, may prevent oocyte damage through antioxidant properties.8–10

Although several environmental chemicals have been associated with decreased fecundability or a longer time-to-pregnancy (TTP),11–15 the impact of metals on TTP and infertility needs further investigation. The effect of lead is of particular interest, given its high toxicity at high levels of exposure in almost every organ. At current environmental levels of exposure, the most notable and strongest association observed with lead exposure is its detrimental effect on children’s neurological function.16, 17 The existing body of research exploring the relationship between female fecundity and lead exposure is limited, and the findings are inconclusive.18–21 Further investigation is warranted to provide a clearer understanding of a potential association.

Two previous cohort studies have investigated the effect of metals on TTP. The New York Angler Cohort, a prospective cohort study including 80 women, reported that higher pre-pregnancy levels of magnesium were associated with a shorter TTP and zinc exposure was associated with a longer TTP, but there was no association for arsenic, cadmium or lead.20 The Longitudinal Investigation of Fertility and the Environment (LIFE) study assessed the effects of environmental chemicals and human fecundity among 501 couples in Michigan and Texas.21 Male lead and female cadmium concentrations were associated with reduced fecundability. When jointly modelling couples’ exposures, only male lead concentration significantly reduced fecundability.21 The few studies that have assessed the impact of environmental metals exposure on infertility (i.e. inability to conceive after 12 months of unprotected intercourse) have reported associations with infertility at increased levels of cadmium or lead.22–24

This study aims to evaluate the association between selected metals (arsenic, cadmium, lead, manganese and mercury), TTP and infertility in participants from the Maternal–Infant Research on Environmental Chemicals (MIREC) study, a Canadian pregnancy and birth cohort.

RESULTS

A total of 1784 participants from the MIREC study met our eligibility criteria (Figure 1). The distribution of demographic and lifestyle characteristics of the study population and their association with TTP are presented in Table 1. Mean maternal age at interview was 32.2 ± 5.0 years and mean gestational age at the time of the blood sample was 11.6 ± 1.6 weeks (± SD). Participants in this study were mostly White, born in Canada, lifelong non cigarette smokers and had a normal pre-pregnancy BMI. Almost two-thirds had an undergraduate degree or higher, more than one-third reported a household income greater than Can$ 100 000, and over half had one previous pregnancy with a live birth.

Details are in the caption following the image
FIGURE 1Open in figure viewerPowerPoint Cohort selection of MIREC study participants.

TABLE 1. Characteristics of 1784 women from the MIREC study, 2008–2011, and association with time-to-pregnancy.

n (%)Time-to-pregnancy (months)Crude FOR (95% CI)
Mean ± SDMedian (IQR)
Maternal age (years)
≤29524 (29.4)3.8 ± 6.91 (1–4)1.00
30–34650 (36.4)4.6 ± 7.42 (1–4)0.81 (0.70–0.94)
35+610 (34.2)7.0 ± 12.82 (1–6)0.62 (0.54–0.72)
Pre-pregnancy BMI (kg/m2)
<24.91052 (59.0)4.8 ± 8.61 (1–4)1.00
25–29.9362 (20.3)5.2 ± 10.71 (1–4)1.03 (0.89–1.21)
>30245 (13.7)6.6 ± 11.11 (1–7)0.76 (0.64–0.91)
Missing125 (7.0)5.2 ± 10.61 (1–4)1.03 (0.82–1.31)
Education
Some college or less281 (15.8)5.1 ± 9.81 (1–5)1.00
College diploma378 (21.2)5.7 ± 10.22 (1–6)0.88 (0.73–1.08)
Undergraduate655 (36.7)5.5 ± 10.82 (1–5)0.96 (0.81–1.15)
Graduate (MSc, PhD)470 (26.3)4.4 ± 6.62 (1–4)1.02 (0.84–1.23)
Income (Can$)
<Can$ 60 000374 (21.0)4.0 ± 6.91 (1–4)1.00
Can$ 60 001–Can $ 100 000624 (35.0)5.4 ± 10.12 (1–5)0.81 (0.69–0.96)
>Can$ 100 000702 (39.3)5.6 ± 10.22 (1–5)0.77 (0.66–0.91)
Missing84 (4.7)5.0 ± 10.72 (1–4)0.90 (0.66–1.22)
Country of birth
Foreign336 (18.8)5.0 ± 8.02 (1–6)1.00
Canada1448 (81.2)5.2 ± 9.92 (1–5)1.04 (0.90–1.21)
Race and ethnicity
White1487 (83.4)5.1 ± 9.72 (1–5)1.00
Not White297 (16.6)5.4 ± 8.92 (1–6)0.93 (0.79–1.08)
Maternal cigarette smoking
Never1087 (60.9)5.1 ± 8.82 (1–5)1.00
Former491 (27.5)5.3 ± 10.82 (1–4)1.06 (0.92–1.21)
Current206 (11.5)5.1 ± 10.22 (1–4)1.09 (0.90–1.32)
Parity
Nulliparous850 (47.6)6.1 ± 11.32 (1–6)1.00
Parous934 (52.4)4.4 ± 7.62 (1–4)1.19 (1.06–1.34)
Total plasma lipids (g/L)
<5.60537 (30.1)4.2 ± 7.82 (1–4)1.00
5.60–6.60613 (34.4)5.0 ± 8.92 (1–5)0.86 (0.74–1.00)
>6.60619 (34.7)6.2 ± 11.42 (1–6)0.75 (0.65–0.87)
Missing15 (0.8)6.5 ± 9.72 (1–6)0.62 (0.32–1.20)
  • Abbreviations: BMI, body mass index; CI, confidence interval; FOR, fecundity odds ratio; IQR, interquartile range; SD, standard deviation.

The cumulative conception rate was 44.8% at 1 month, 81.9% at 6 months and 90.8% at 12 months. Hence, the rate of infertility (TTP > 12 months) in this cohort was 9.2%. Maternal age, pre-pregnancy BMI, income, parity and total plasma lipids were associated with TTP (Table 1). Older women, with higher BMI, higher income or increased plasma lipids had decreased fecundability (longer TTP). Parous women had a shorter TTP. Education, country of birth, race and ethnicity, and cigarette smoking status were not associated with TTP (Table 1).

Most participants had detectable blood levels of all five metals (Table 2). Geometric means for arsenic, cadmium, lead, manganese and mercury were 0.73 μg/L, 0.21 μg/L, 0.62 μg/dL, 8.79 μg/L and 0.61 μg/L, respectively. TABLE 2. Whole blood concentrations of metals, MIREC study 2008–2011.

LODn (%) < LODMedianMinimumMaximumGM (95% CI)
Arsenic (μg/L)0.23136 (7.62)0.83<LOD34.590.73 (0.71–0.76)
Cadmium (μg/L)0.0447 (2.63)0.20<LOD5.50.21 (0.20–0.22)
Lead (μg/dL)0.100 (0)0.630.165.210.63 (0.61–0.64)
Manganese (μg/L)0.55173 (9.70)8.792.0329.128.80 (8.67–8.93)
Mercury (μg/L)0.12153 (9.74)0.70<LOD10.030.61 (0.58–0.64)
  • Abbreviations: CI, confidence interval; GM, geometric mean; LOD, limit of detection.

In relation to TTP, increments of one SD increase in blood concentrations of arsenic, cadmium, manganese or mercury were not associated with TTP (Table 3). In the adjusted model, increments of one SD of lead concentrations resulted in a shorter TTP (adjusted FOR [aFOR] 1.09; 95% CI 1.02–1.16). When exposure was modelled as tertiles, no relationship was observed between arsenic, cadmium, manganese or mercury and TTP. For lead, relative to the first tertile, the second (aFOR 1.33; 95% CI 1.14–1.54) and third (aFOR 1.28; 95% CI 1.10–1.50) tertiles were associated with a shorter TTP (Table 3). TABLE 3. Fecundability odds ratios for the association between metals and time-to-pregnancy, MIREC study 2008–2011.

MetalsLevelsnCrude FOR (95% CI)Adjusted FORa (95% CI)
Arsenic (μg/L)log2As/SD17840.99 (0.94–1.05)1.02 (0.95–1.08)
<0.606001.001.00
0.60–1.055960.93 (0.80–1.07)0.94 (0.81–1.10)
>1.055880.96 (0.83–1.11)0.99 (0.85–1.17)
Cadmium (μg/L)log2Cd/SD17841.02 (0.97–1.09)1.04 (0.97–1.12)
<0.155681.001.00
0.15–0.285901.06 (0.92–1.23)1.10 (0.94–1.27)
>0.286261.06 (0.91–1.22)1.07 (0.91–1.26)
Lead (μg/dL)log2Pb/SD17841.06 (1.00–1.13)1.09 (1.02–1.16)
<0.505751.001.00
0.50–0.775781.27 (1.10–1.48)1.33 (1.14–1.54)
>0.776311.24 (1.04–1.43)1.28 (1.10–1.50)
Manganese (μg/L)log2Mn/SD17841.02 (0.96–1.08)1.04 (0.98–1.10)
<7.696401.001.00
7.69–10.445761.10 (0.96–1.28)1.12 (0.96–1.29)
>10.445681.11 (0.96–1.28)1.17 (1.01–1.35)
Mercury (μg/L)log2Hg/SD17840.94 (0.89–1.00)0.98 (0.92–1.05)
<0.425941.001.00
0.42–1.045860.87 (0.75–1.00)0.92 (0.79–1.07)
>1.046040.87 (0.75–1.01)0.95 (0.81–1.11)
  • Note: FOR derived from Cox proportional hazards model modified for discrete time data with multiple imputation (m = 20) for missing covariate information.
  • Abbreviations: CI, confidence interval; FOR, fecundity odds ratio.
  • a Adjusted for maternal age, pre-pregnancy body mass index, education, income, country of birth, race and ethnicity, maternal cigarette smoking, plasma lipids and recruitment site.

In relation to infertility (TTP > 12 months), increments of one SD increase of blood concentrations of arsenic, cadmium, lead, manganese or mercury were not associated with infertility (Table 4). When modelled as tertiles, exposures to arsenic, cadmium or mercury were not associated with infertility. For lead, relative to the first tertile, the second tertile was associated with decreased odds of infertility (aOR 0.57; 95% CI 0.37–0.87), but not the third tertile (Table 4). For manganese, relative to the first tertile, no association was observed with the second tertile, but the third tertile was associated with decreased odds of infertility (aOR 0.64; 95% CI 0.42–0.96) (Table 4). TABLE 4. Odds ratios for the association between blood metals and infertility, MIREC study 2008–2011.

MetalsLevelsnCrude OR (95% CI)Adjusted ORa (95% CI)
Arsenic, μg/Llog2As/SD17841.14 (0.96–1.34)1.13 (0.95–1.35)
<0.606001.001.00
0.60–1.055961.32 (0.88–1.98)1.32 (0.86–2.00)
>1.055881.29 (0.86–1.94)1.27 (0.82–1.97)
Cadmium, μg/Llog2Cd/SD17840.99 (0.84–1.17)0.95 (0.77–1.17)
<0.155681.001.00
0.15–0.285900.98 (0.66–1.46)0.89 (0.56–1.35)
>0.286260.99 (0.67–1.47)0.94 (0.60–1.47)
Lead, μg/dLlog2Pb/SD17840.91 (0.77–1.07)0.87 (0.73–1.04)
<0.505751.001.00
0.50–0.775780.61 (0.40–0.92)0.57 (0.37–0.87)
>0.776310.79 (0.54–1.16)0.73 (0.48–1.10)
Manganese, μg/Llog2Mn/SD17840.91 (0.78–1.07)0.86 (0.72–1.02)
<7.696401.001.00
7.69–10.445760.75 (0.51–1.11)0.74 (0.50–1.10)
>10.445680.71 (0.48–1.06)0.64 (0.42–0.96)
Mercury, μg/Llog2Hg/SD17841.20 (1.01–1.42)1.09 (0.90–1.33)
<0.425941.001.00
0.42–1.045861.41 (0.93–2.13)1.20 (0.78–1.85)
>1.046041.44 (0.96–2.16)1.16 (0.74–1.83)
  • Note: Odds ratios derived from multiple logistic regression analysis with multiple imputation (m = 20) for missing covariate information.
  • Abbreviations: CI, confidence interval; OR, odds ratio.
  • a Adjusted for maternal age, pre-pregnancy body mass index, education, income, country of birth, race and ethnicity, maternal cigarette smoking, plasma lipids and recruitment site.

In the sensitivity analysis stratified by parity (Table S1), the association between lead and shorter TTP remained among nulliparous (aFOR 1.10; 95% CI 1.01–1.21), and parous (aFOR 1.09; 95% CI 1.00–1.19) women. When including parity in the adjusted model (Table S2), results were similar to the main analysis presented in Table 3. The sensitivity analysis stratified by manganese levels yielded similar results in terms of FOR, except for lead where a slight attenuation in the 95% CI occurred in those with manganese concentration above the median (Table S3).

4 DISCUSSION

4.1 Main findings

In this pregnancy-based retrospective TTP cohort study in participants from the Canadian MIREC study, environmental exposure to arsenic, cadmium, manganese and mercury measured during the first trimester were not associated with TTP or infertility. Exposure to lead was associated with a shorter TTP, but the pattern of effect was not consistent with a dose–response relationship.

4.2 Strengths and limitations

The major strengths of this study include its large sample size and the use of biomarkers as an objective measure of total metal exposure. The limitations of this research are related to the retrospective assessment of exposure and outcome, residual confounding and an underlying cohort of women who became pregnant, and therefore excluded those with infertility who did not access fertility treatment or were not successful after treatment.

The measurement of exposure was taken during the first trimester of pregnancy as a proxy for pre-conception exposure. The accuracy of this measure is impacted by the stability of participant’s behaviour in relation to metal exposures, and by physiological changes during pregnancy. Both sources of error would contribute to non-differential exposure measurement error in this study and would tend to bias effect estimates towards the null, given that the measurement of exposure was collected during the first trimester of pregnancy in all participants independent of TTP. Furthermore, most of the metals included have a relatively long half-life (3–4 months for cadmium,34 90 days for lead,35 2–5 weeks for manganese36–38 and 44–80 days for mercury39–41), except for arsenic, which has a half-life of only several hours.42 However, with continuous exposure, concentrations may reach a steady state.33 Concerning the outcome, TTP was collected by questionnaire and relies on subject recall. However, the collection of retrospective TTP is a reliable method when data are collected in the short term, as was the case in the MIREC study.43

There is also the potential for residual confounding, due to the unavailability of some data in the MIREC study, such as menstrual cycle regularity, associated gynaecological conditions and coital frequency. The absence of sociodemographic and biomonitoring data for the male partner in the MIREC study is another limitation. For example, the LIFE study reported that male partners’ metal concentrations were more often associated with reduced couple fecundability compared with female partners’ concentrations.44

In addition, the study population was restricted to women who have had a birth and/or became pregnant, inherently conditioning on fertility. This introduces the potential for collider bias, which occurs when exposure and outcome each influence a common third variable, and that variable is conditioned on in the design or analysis.45 In the MIREC study, participants are restricted to those who have had a birth. Both the exposure (lead) and outcome influence fertility status and could therefore produce a collider bias because the study population has been restricted to those able to conceive.46, 47 However, biologically, there is a wide range of reproductive capacity, even among couples who achieve pregnancy. This heterogeneity is expressed in the gradual decrease in conception rates during successive months of trying,47, 48 which is not a true time effect, but evidence of sorting among individuals who are heterogeneous in their capacity to conceive.48 Heterogeneity among couples raises the possibility that some of this variation may be explained by identifiable factors, supporting the rationale of our study. Finally, as the MIREC cohort consists mainly of healthy mothers of moderate to high socioeconomic status, and Caucasian race and ethnicity,25 metal concentrations and other factors associated with TTP might differ from other populations, limiting the external generalisability of our results.49

4.3 Interpretation

Two studies have evaluated the relationship between metals and TTP, and both were prospective cohort studies of pre-conception couples. The LIFE Study observed a reduction in couple fecundity with higher exposure to cadmium and lead. When assessing individual partner exposure, female cadmium exposure (aFOR 0.78, 95% CI 0.63–0.97) and male lead exposure (aFOR 0.85, 95% CI 0.73–0.98) were associated with a longer TTP. No association was observed with mercury. Except for mercury, geometric mean concentrations of blood metals in MIREC participants (0.21 μg/L for cadmium, 0.62 μg/dL for lead and 0.61 μg/L for mercury) were similar to those reported in the LIFE study (0.21 μg/L for cadmium, 0.66 μg/dL for lead and 0.98 μg/L for mercury).21 The prospective design of the LIFE study, and the difference in sociodemographic characteristics compared with the MIREC study could explain the differences in our results. On the other hand, consistent with our results, the prospective cohort study using preconception enrolment of women from the New York Angler Cohort did not find evidence to support the association between low-level exposure to toxic metals and fecundity, even though the concentrations of metals in the Angler Cohort were higher than in MIREC (4.27 μg/L for arsenic, 1.63 μg/L for cadmium, 1.55 μg/dL for lead).20 However, the small number of participants included in this cohort (n = 80) may have made it underpowered to detect any association.

We remain uncertain about the observed association between lead exposure and a shorter TTP. To our knowledge, no other study has reported a similar finding. The absence of a dose–response when the exposure is modelled as tertiles or restricted cubic splines, suggests a spurious association, which could be a result of the above-mentioned limitations of our study. To further explore this association, we investigated the potential impact of gestational age at the time of sample collection on the association between lead exposure and TTP. This exploration was motivated by the understanding that blood lead concentrations encompass both ongoing exposure and lead stores in bone.50 During pregnancy, heightened calcium demands induce increased bone turnover, leading to the release of lead from bone and subsequent increase in blood lead levels.50–52 Our hypothesis posited a reduced fecundability (longer TTP) for metals in women’s samples collected after 10 weeks of gestation. However, we were not able to demonstrate this, as lead continued to be associated with a shorter TTP independent from the gestational age at the time of interview.

Regarding infertility, authors of an analysis among 124 participants of the 2013–2014 and 2015–2016 National Health and Nutrition Examination Surveys (NHANES) reported an association between log-transformed blood lead (OR 2.60, 95% CI 1.05–6.41) and cadmium (OR 1.84, 95% CI 1.07–3.15) and self-reported infertility.22 The geometric mean of blood lead was lower in this study (0.50 μg/dL) compared with MIREC; however, the geometric mean of blood cadmium (0.26 μg/L) was similar. Another study including a larger sample of 838 participants from the 2013–2018 NHANES reported no association between blood concentrations of cadmium or mercury and self-reported infertility.23 Lead concentrations were associated with infertility in some categories but with no overall dose–response pattern.23 Compared with MIREC, mean concentrations of cadmium and mercury in NHANES were higher (0.45 μg/L for cadmium, 1.15 μg/L for mercury); however, concentrations of lead were the same (0.70 μg/dL). We found a decreased odds of infertility in the second tertile (0.50–0.77 μg/dL) of exposure for lead (OR 0.52, 95% CI 0.33–0.84), but not in those in the highest tertile (>0.77 μg/dL) or when the exposure was modelled as a continuous variable.

5 CONCLUSION

Our study supports the theory that at current environmental levels of exposure, which are low relative to levels seen in other populations, metals are not associated with decreased fecundability or infertility. Further studies are needed to assess the role of lead, if any, on TTP and infertility.

Humanized mice reveal arsenic may raise diabetes risk only for males

Posted by

0


Chronic exposure to arsenic, often through contaminated groundwater, has been associated with Type 2 diabetes in humans, and there are new clues that males may be more susceptible to the disease when exposed.

A new study – using lab mice genetically modified with a human gene to shed light on the potential link – revealed that while the male mice exposed to arsenic in drinking water developed diabetes, the female mice did not.

These results would not have been possible without using a mouse model engineered to express a human enzyme for metabolizing arsenic, since normal mice process arsenic much more efficiently than humans and require very high levels of exposure before they become diabetic.

In the paper, the researchers also identified a transcription factor called Klf11, which might be the master regulator of the difference in how the livers of males and females respond to arsenic.

“Our paper lays the foundation for future investigations into the mechanism of how arsenic exposure leads to diabetes, why there are striking male-female differences, and potential therapeutic strategies,” said Praveen Sethupathy ’03, professor of physiological genomics and chair of the Department of Biomedical Sciences at the College of Veterinary Medicine, and the study’s senior author.

“It highlights how important it is to use an appropriate genetic model [in this case, humanized mice], because none of these results were seen in the wild-type mice,” said Jenna Todero, a doctoral student in Sethupathy’s lab.

Todero is the first author of “Molecular and Metabolic Analysis of Arsenic-exposed Humanized Arsenic +3 Methyl Transferase (AS3MT) Mice,” which published Dec. 27 in the journal Environmental Health Perspectives.

Arsenic is the top priority substance for study, according to the Agency for Toxic Substances and Disease Registry. Human exposure to arsenic, which is common in the environment, often comes through contaminated groundwater. The safe exposure limit is 10 parts per billion, according to the World Health Organization and the Environmental Protection Agency.

Endemic levels of arsenic above safe limits in both Bangladesh and Mexico led to studies that showed an association between higher levels of arsenic exposure and Type 2 diabetes. Though these studies had very small sample sizes, they offered clues for further research.

The current study was performed on regular lab mice – known as wild-type mice – as a control and humanized mice that were engineered to express a human form of an enzyme, AS3MT, which is found across species, and is important for metabolizing arsenic in the body. Efficiency of this enzyme differs across species, but mice are far faster than humans at metabolizing arsenic.

All the mice were exposed for a month to doses of arsenic in drinking water that were nonlethal but sufficient to potentially promote Type 2 diabetes. The researchers then examined liver and white adipose tissues that are implicated in diabetes. In the humanized male mice alone, they found increased expression in genes related to insulin resistance. Also, in both liver and white adipose tissues of the humanized male mice, they identified a biomarker called miR-34a, which is highly associated with insulin resistance in Type 2 diabetes and other metabolic diseases.

“This would suggest miR-34a is potentially a way to screen individuals who live in areas that have endemic arsenic levels,” Todero said. “If you have elevated miRNA-34a, you might be at risk for Type 2 diabetes onset or other metabolic dysfunction.”

The researchers also identified the transcription factor (which regulates genes) Klf11 in the liver. “This was really exciting because we showed that genes that are highly important for things like regulating glucose or lipid metabolism seem to be targets for Klf11,” Todero said.

They found that Klf11 was significantly turned down in the humanized males, but not in the wild-type mice or the females. The study’s authors speculate that Klf11 might be a master regulator for genes associated with energy usage. It was suppressed in humanized male mice, likely causing dysregulation, and hallmarks of diabetes such as insulin resistance and elevated fasting blood glucose.

In the female humanized mice, the researchers found evidence of elevated expression of genes that support insulin sensitivity.

“We saw the opposite effect in females, where genes that promoted insulin sensitivity and glucose uptake had their expression increased,” Todero said. Previous work by another group suggested that the female sex hormone estradiol may play a role in the sexual divergence in the association between arsenic and Type 2 diabetes.

Arsenic exposure linked to early puberty, obesity

Posted by

0


Exposure to low levels of arsenic through drinking water in utero resulted in signs of early puberty and obesity as adults in female mice, according to recent findings.

“We unexpectedly found that exposure to arsenic before birth had a profound effect on onset of puberty and incidence of obesity later in life,” Humphrey Yao, PhD, a reproductive biologist at the National Institute of Environmental Health Sciences (NIEHS), said in the release. “Although these mice were exposed to arsenic only during fetal life, the impacts lingered through adulthood.”

Currently, the Environmental Protection Agency states that the maximum allowable amount for arsenic in drinking water is 10 parts per billion.

The researchers divided female mice into three groups: control (no exposure), standard exposure (current EPA guideline) or high level (42.5 parts per billion). Exposure occurred during gestation, between 10 days after fertilization and birth corresponding to the middle of the first trimester and birth in humans.

The researchers found that both the high and low doses resulted in weight gain as well as onset of puberty.

“It’s very important to study both high doses and low doses,” Linda Birnbaum, PhD, director of NIEHS and the National Toxicology program, said in the release. “Although the health effects from low doses were not as great as with extremely high doses, the low-dose effects may have been missed it only high doses were studied.”

Low-level arsenic exposure may impair insulin sensitivity

Posted by

0


Urinary total arsenic levels in a group of nondiabetic Amish adults are associated with insulin sensitivity, but are not linked to beta-cell function measures, according to study data published in Diabetes/Metabolism Research and Reviews.

Sung Kyun Park, ScD, MPH, of the University of Michigan School of Public Health, and colleagues analyzed data from 221 adults without diabetes and normal glucose tolerance (n = 164) or impaired glucose tolerance (n = 57) participating in the Amish Family Diabetes study, a genetic epidemiology study of type 2 diabetes in Old Order Amish living in Lancaster, Pennsylvania. Participants were recruited between 1995 and 1998 (mean age, 53 years; 115 women). All participants underwent a 75 g oral glucose tolerance test and fasting blood sample to measure insulin sensitivity and beta-cell function; researchers also measured urinary arsenic concentrations. All arsenic concentrations among the participants were above the limit of detection (0.1 µg/L). To account for correlations among sibling participants, researchers used generalized estimating equations with an exchangeable correlation structure.

Urinary total arsenic was significantly and inversely associated with two insulin sensitivity measures after adjusting for age, sex, urinary creatinine and adiposity (Stumvoll metabolic clearance rate = –0.23 mg/[kg x min]; 95% CI, –0.38 to –0.09; Stumvoll insulin sensitivity index = –0.0029 mol/[kg x min x pM]; 95% CI, –0.0047 to –0.0011).

Urinary total arsenic also was significantly associated with higher fasting glucose levels (0.57 mg/dL per interquartile range increase; 95% CI, 0.06-1.09).

Researchers did not find a significant association between urinary arsenic and beta-cell function measures.

“Notably, these associations were stronger and remained statistically significant following covariate adjustment compared to the widely used index of insulin resistance, HOMA-IR, which is based on fasting measures of insulin and glucose,” the researchers wrote. “Previous mixed results may be partly due to low sensitivity of HOMA-IR.”

FDA Finally Admits Chicken Meat Contains Cancer-Causing Arsenic

Posted by

1


The FDA spent years trying to hide the issue, hoping that no one would go further with the subject. However, they finally admitted that the chicken sold all over the United States contains a toxic chemical called arsenic, known to cause cancer, and in high doses it is fatal.

What is even more horrible is the story explaining how does the chemical get in the chicken: It is added to their feed.Actually chickens are fed with it purposely!

The FDA confirmed that in their own research they found that the arsenic in the chicken feed really finishes in the meat that is later consumed by people. More precisely, in the last 60 years all the Americans that consumed conventional chicken have actually been consuming this cancer-causing chemical called arsenic!

After all those dark years of denial,the latest study brought light that arsenic actually ends up in the meat because it is being added to the chicken feed. We have to mention that both the FDA and the poultry industry denied this fact.FDA

For sixty years we have been believing in the fairy tale that “the arsenic is excreted in the chicken feces.” It is just a vain story presented by the poultry industry, and it was never backed up with scientific evidence. And we had to believe in it.

Some manufacturers, including the manufacturer of the chicken feed product known as Roxarsone,now that the world knows this undeniable evidence, has decided to withdraw all of their products off the supermarket shelves.

Interesting fact is that, the manufacturer that is adding the arsenic into the chicken feed is Pfizer. This is the same company that produces vaccines containing chemical adjuvants that are later used to inject children.

The company producing the Roxarsone chicken feed is called Alpharma LLC, and it is actually a subsidiary of Pfizer. Alpharma now decided to withdraw their products from the shelves all over the US, and they also saidthat there is no need to necessarily withdrawtheir products in other countries unless the regulators say otherwise. AP reported that:

“Pfizer Animal Health’s Veterinary Medicine Research and Development division, Scott Brown said that the company is also selling the ingredient in many other countries. He also said that Pfizer is contactingthe regulatory authorities in those countries and will decide if they are going to sell it on an individual basis.”

The FDA still denies these facts,even though the arsenic-containing products are pulled off the shelves, they claim that the chicken is safe for consumption as the arsenic in the meat is at a low level. It seems like thereis not going to be any changes regarding this subject, even though the FDA stated that the arsenic is a carcinogenous substance, which means that it increases the risk of cancer.

Even the National Chicken Council agrees with the FDA. As a response to the decision that Roxarsone’s products must be withdrawn from the shelves,in a statement they said, “The chicken is safe for consumption,” despite admitting the fact that the chemical is added in the chicken feed and the meat is later sold all over the United States.

We are shocked that the FDA still tells the consumers that it is safe to eat the arsenic-loaded chicken but it is dangerous to drink elderberry juice! The FDA recently conducted an armed raid and accused an elderberry juice manufacturer of the “crime” of selling “unapproved drugs”.

And what kind of drug would that be? The elderberry juice, explained the agency. The elderberry juice is considered as a “drug”, as you can see, at the very moment you tell people how it can improve their overall health.

Dozens of other manufacturers were also attacked by the FDA,for selling natural nutritional products or herbal products with a scientific back up that proves their ability to support and enhance health. The agency goes that far to say that even raw milk is dangerous. In other words, the food and drug regulatory agency in America says that it is dangerous to drink elderberry juice or raw milk, but approves the consumption of arsenic.

Surprising Source of Arsenic in Your Drinking Water—Will EPA Take Steps to Protect Your Health?

Posted by

0


Story at-a-glance

  • While naturally-occurring arsenic in groundwater is one of the most common sources of exposure, hydrofluorosilicic acid (fluoride) added to drinking water is commonly contaminated with toxic arsenic
  • According to recent research, diluted fluorosilic acid adds, on average, about 0.08 ppb of arsenic to your drinking water
  • Low-level chronic exposure to arsenic can lead to a wide variety of health problems, including chronic fatigue, reproductive problems, reduced IQ and other neurological problems, and various cancers
  • As petition urges the EPA to change the source of fluoride in US drinking water, as the most commonly used form, hydrofluorosilicic acid, increases lung and bladder cancer risk
  • Switching from hydrofluorosilicic acid to pharmaceutical-grade fluoride could save the US $1-6 billion annually and prevent an estimated 1,800 cases of lung and bladder cancer

Pure water is one of the most important foundations for optimal health.Unfortunately, most tap water is far from pure, containing a vast array ofdisinfection byproducts, chemicals, heavy metals and even pharmaceutical drugs.Fluoride and arsenic are two prime examples of hazardous water contaminants.

Image

Not only is the level of arsenic in US tap water high due to natural groundwater contamination,1 the most commonly used form of fluoride added to water supplies also tends to be contaminated with arsenic. As reported by the featured article:2

“In early August, the Environmental Protection Agency is set to decide on a petition to change the source of fluoride in US drinking water.

Currently, the source of fluoride in most public water supplies isfluorosilicic acid, according to government records. The petition calls for the EPA to instead require the use of pharmaceutical-grade sodium fluoride in water fluoridation, which is the addition of fluoride to drinking water for the purpose of preventing cavities.

Fluorosilicic acid is often contaminated with arsenic, and recent research has linked the arsenic from fluorosilicic acid in drinking water to as many as 1,800 extra cases of cancer yearly in the United States…”

The petition3 was submitted by William Hirzy, a chemistry researcher at the American University in Washington, D.C. Hirzy previously worked at the EPA for 27 years.

His team recently published a study entitled: Comparison of hydrofluorosilicic acid and pharmaceutical sodium fluoride as fluoridating agents – a cost-benefit analysis, in the journal Environmental Science & Policy.4

According to their estimation, switching the type of fluoride used to pharmaceutical-grade sodium fluoride would reduce the amount of inorganic arsenic contamination in drinking water by 99 percent!

The Health Dangers of Inorganic Arsenic

Inorganic arsenic is a powerful carcinogen that has been linked to an increased risk of several types of cancer. In 2001 the Environmental Protection Agency(EPA) lowered the maximum level of arsenic permitted in drinking water from 50 ug/L to 10 ug/L (or 10 parts per billion (ppb)) due to the established cancer risk.

The Natural Resources Defense Council5 estimates that as many as 56 million Americans living in 25 states drink water with arsenic at unsafe levels. According to the EPA:6

“Chronic inorganic arsenic exposure is known to be associated with adverse health effects on several systems of the body, but is most known for causing specific types of skin lesions (sores, hyperpigmentation, and other lesions) and increased risks of cancer of the lungs and skin.”

Other impacts of chronic arsenic exposure include, according to the EPA:

Kidney damage and failure Anemia Low blood pressure
Shock Headaches Weakness
Delirium Increased risk of diabetes Adverse liver and respiratory effects, including irritation of mucous membranes
During development, increased incidence of preterm delivery, miscarriage, stillbirths, low birth weight, and infant mortality During childhood, decreased performance in tests of intelligence and long-term memory Skin lesions

Water Fluoridation Chemicals Are NOT Pharmaceutical Grade

While naturally-occurring arsenic in groundwater is one of the most common sources of exposure, hydrofluorosilicic acid—the most commonly used form of fluoride added to water supplies—is a toxic waste product from the phosphate fertilizer industry that is commonly contaminated with arsenic, radionucleotides, aluminum and other industrial contaminants.

According to the featured research, diluted fluorosilic acid adds, on average, about 0.08 ppb of arsenic to your drinking water.

Most people are shocked when they realize that the fluoride added to their water supply is actually a toxic byproduct from the fertilizer industry, opposed to a pharmaceutical-grade chemical. The source of most water fluoridation chemicals is explained by Michael Miller, a minerals commodity specialist for the US Geological Survey, in the featured article:7

“During the production of phosphate fertilizer, phosphate ore is reacted with sulfuric acid to produce toxic gases. These are taken out of the air after being sprayed with water, which produces fluorosilicic acid… The solution is sold to water systems nation-wide, where it is diluted and put into drinking water. Occasionally, it is treated to create sodium fluorosilicate. Together, these compounds (called silicofluorides) provide fluoride to 90 percent of U.S. drinking water systems that are fluoridated…”

Water Fluoridation May Be Placing Infants at Great Risk

Not only is there mounting evidence that fluoride poses grave health risks to infants and children—including reductions in IQ—arsenic exposure in utero and during early childhood is also particularly problematic, as it can cause lasting harm to children’s developing brains, and endocrine- and immune systems.

For example:

  • A 2006 study8 found that Chileans exposed to high levels (peaking at 1,000 ppb) of naturally-occurring arsenic in drinking water in utero and during early childhood had a six times higher lung cancer death rate compared to Chileans living in areas with lower levels of arsenic in their water. And their mortality rate in their 30s and 40s from another form of lung disease was almost 50 times higher than for people without that arsenic exposure.
  • A 2004 study9 showed children exposed to arsenic in drinking water at levels above 5 ppb had lower IQ scores. Earlier studies have linked chronic arsenic exposure to a range of cognitive dysfunctions, including learning disabilities, memory problems, poor concentration, and peripheral and central neuropathies.
  • A study10 published in 2011 examined the long-term effects of low-level exposure on more than 300 rural Texans whose groundwater was estimated to have arsenic at median levels below the federal drinking-water standard. It also found that exposure was related to poor scores in language, memory, and other brain functions.

Is It Worth Increasing Cancer Risk for Minimal, if Any, Benefit to Teeth?

Some proponents of fluoridation believe that the large dilution of these fluoridating chemicals that takes place when they are added at the public water works ameliorates concerns about the known contaminants. However, arsenic is a known human carcinogen, for which there is no safe level.

Inevitably, the addition of contaminated hexafluorosilicic acid to the water supply by definition must increase the cancer rate in the US because of the arsenic it contains, and this is exactly what Hirzy’s research shows. Why would any rational government do that to reduce – at best – a miniscule amount of tooth decay? According to Hirzy:11

“We found that the United States as a society is spending, conservatively speaking, $1 billion to $6 billion treating the excess bladder and lung cancers caused by arsenic in the most commonly used fluoridation chemical, fluorosilicic acid… The switch [to pharmaceutical-grade sodium fluoride] would cost $100 million, but would save billions in reduced cancer costs.”

For people living in areas with fluoridated tap water, fluoride is a part of every glass of water, every bath and shower, and every meal cooked using that water. This makes absolutely no sense considering the carcinogenic nature of arsenic—especially in light of the epidemic of cancer.

Hirzy’s study is actually the first risk assessment of arsenic-contaminated fluoride in drinking water. This is particularly shocking considering the fact that fluorosilicic acids have been used since the early 1950’s12 (prior to that, sodium fluoride, a byproduct of the aluminum industry, was typically used). Incredibly, while the EPA performs risk assessments for most drinking water contaminants, the agency does NOT oversee the addition of fluoridation chemicals. As stated in the featured article, this policy makes no sense whatsoever.

“Under the Toxic Substances Control Act, the EPA has the authority to regulate or ban almost any substance — including fluorosilicic acid — that poses an ‘unreasonable risk’ to public health, [Hirzy] said.”

Appropriations Bill Would Prohibit EPA’s Phase-Out of Sulfuryl Fluoride

While we’re on the topic of fluoride, a related news item13 is worthy of note. Drinking water is not the only source of fluoride, as I’ve discussed previously. Fluoride also enters the human food chain via fluoridated pesticides. According to a recent report, the House of Representatives Appropriations Interior and Environmental subcommittee has voted to approve an appropriations bill that cuts the EPA’s budget by nearly one-third.

What’s worse, the bill specifically prevents the EPA from enforcing its decision to phase out sulfuryl fluoride—a neurotoxic fumigant that has been linked to cancer and neurological-, developmental-, and reproductive damage. If it passes once markups by the Appropriations Committee are completed, it will move to a House vote. According to the news report:

“This is an outrageous attempt to circumvent a basic risk assessment calculation that EPA acknowledges puts the public at risk, given current exposure patterns, to a chemical that is especially hazardous to children.”

In response, Beyond Pesticides, the Environmental Working Group (EWG), and the Fluoride Action Network (FAN) submitted a letter14 to the House Appropriation Committee Chairman and Ranking members, urging them to remove the section in question (section 449) from the bill. You can help by writing or calling your state Representative, asking him or her to uphold the EPA’s ability to protect the health of all Americans by removing this hazardous pesticide from our food production. There’s no need for it, as there are many other viable alternatives, including:

  • Temperature manipulation (heating and cooling)
  • Atmospheric controls (low oxygen and fumigation with carbon dioxide)
  • Biological controls (pheromones, viruses and nematodes)
  • Less toxic chemical controls, such as diatomaceous earth

Water Filtration – A Must for Clean Pure Water…

If you have well water, it would be prudent to have your water tested for arsenic and other contaminants. If you have public water, you can get local drinking water quality reports from the EPA.15

In general, most water supplies contain a number of potentially hazardous contaminants, from fluoride, to drugs and disinfection byproducts (DBP’s), just to name a few. You can get a good idea of what types of contaminants could be in your drinking water right now by viewing this awesome graphic from GOOD Environment16 (reprinted with permission.) It gives you a look at the five most and least polluted water systems in America (in cities with more than 100,000 population), including pointing out the pollutants of largest concern.

I strongly recommend using a high quality water filtration system unless you can verify the purity of your water. To be absolutely certain you are getting the purest water you can, you’ll want to filter the water both at the point of entry and at the point of use. This means filtering all the water that comes into the house, and then filtering again at the kitchen sink. I currently use a whole house carbon-based water filtration system, and prior to this I used reverse osmosis (RO) to purify my water.

You can read more about water filtration in this previous article to help you make a decision about what type of water filtration system will be best for you and your family. Since most water sources are now severely polluted, the issue of water filtration and purification couldn’t be more important.

Ideal Water Sources

Besides purification, I also believe it’s critical to drink living water. I recently interviewed Dr. Gerald Pollack about his book, The Fourth Phase of Water: Beyond Solid, Liquid, and Vapor. This fourth phase of water is referred to as “structured water” and is the type of water found in all of your cells. This water has healing properties, and is naturally created in a variety of ways.

Water from a deep spring is one excellent source of structured water. The deeper the better, as structured water is created under pressure. There’s a great website called FindaSpring.com17 where you can find a natural spring in your area.

But you can also promote structured water through vortexing. I personally drink vortexed water nearly exclusively as I became a big fan of Viktor Schauberger who did much pioneering work on vortexing about a century ago. Dr. Pollack found that by creating a vortex in a glass of water, you’re putting more energy into it, thereby increasing the structure of the water. According to Dr. Pollack, virtually ANY energy put into the water seems to create or build structured water.

My own R&D team is working on a careful study in which we use vortexed water to grow sprouts, to evaluate the vitality and effectiveness of the water. We are conducting extensive internal research to develop the best vortex machine on the market, because we believe an ideal vortexer could be one of the simplest ways to improve people’s health.

Water Fluoridation Is Anything But Safe…

According to Bill Hirzy, water fluoridation remains a government policy because of “institutional inertia [and] embarrassment among government agencies that have been promoting this stuff as safe.” This is probably true, yet it’s shameful that the practice is allowed to continue in the face of overwhelming evidence showing the health hazards of not just fluoride itself, but also of related contaminants such as arsenic.

Clean pure water is a prerequisite to optimal health. Industrial chemicals, drugs and other toxic additives really have no place in our water supplies.

Source: mercola.com