The Association of Arsenic Metabolism and Blood Pressure: A Cross-

Overview

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Key numbers

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• pressure, pulse pressure, and mean arterial pressure—among 393 participants in the MesoAmerican Nephropathy Occupational Study (MANOS) in El
• vs. lower DMA% (>77.51% vs. ≤71.28% DMA over the sum of inorganic and methylated arsenic species) showed higher systolic blood pressure (β = 3.75
• mmHg; 95% CI: 0.65, 6.85) and pulse pressure (β = 2.57 mmHg; 95% CI: 0.04, 5.10), while participants with higher vs. lower MMA% (>16.07% vs. ≤12.39%)
• showed lower systolic blood pressure (β = ‑3.70 mmHg; 95% CI: ‑6.86, ‑0.55) and pulse pressure (β = -2.76 mmHg; 95% CI: ‑5.33, ‑0.19). In leave-one-out
• models, higher DMA% (>77.51% vs. <71.28%) as a result of lower MMA%, was associated with higher systolic blood pressure (β = 7.24 mmHg; 95% CI: 2.25,
• 12.2), pulse pressure (β = 5.29 mmHg; 95% CI: 1.22, 9.36), and mean arterial pressure (β = 3.71 mmHg; 95% CI: -0.08, 7.50). PCA results supported these
• findings. The second methylation step from MMA to DMA was associated with higher systolic blood pressure (β = 0.93 mmHg; 95% CI: 0.11, 1.75) and pulse
• pressure (β = 0.74 mmHg; 95% CI: 0.07, 1.40).
• World Health Organization’s 10 µg/L guideline for arsenic in drinking water (12-14).
• Of the participants who had an eGFR > 45 mL/min/1.73 m2, only those with urinary total arsenic concentrations >5 µg/L were selected for speciation
• analysis. This resulted in a cohort of 404 participants (71% of all MANOS participants) with speciated arsenic measurements. An additional four participants
• available for this analysis consisted of 393 participants (69%). All participants provided written consent (18).
• The samples were thawed, and an aliquot (100 µL) was treated with hydrogen peroxide (30%wt, 10 µL) solution by volume. The resulting solutions were
• The MDL for InAs was 0.05 µg/L, that of MMA was 0.04 µg/L, and that of DMA was 0.03 µg/L. Any arsenic concentrations below the MDL were imputed with
• MDL⁄√2. All arsenic species were detected in 100% of participants, apart from InAs, which was detected in 98.8% of participants.
• InAs%=(InAs concentration)/(Total arsenic concentration)×100% (Equation 1)
• MMA%=(MMA concentration)/(Total arsenic concentration)×100% (Equation 2)
• DMA%=(DMA concentration)/(Total arsenic concentration)×100% (Equation 3)
• associated with adverse health outcomes (22, 23). Mean arterial pressure (MAP) was calculated using the following equation (24):
• Table 1. Descriptive Statistics of the Participants in the MANOS Cohort.
• Summed Urinary Arsenic2, µg/L 11.0 (11.2) 10.8 (10.7) 11.0 (10.9)
• Urinary InAs, % 11.3 (6.3) 11.1 (6.2) 11.2 (6.2)
• Spearman correlation between DMA% and arsenobetaine levels. In sensitivity analyses, we evaluated (1) the inclusion of the sum of organic and methylated
• Table 2. Conventional Modeling: Linear Regression Results of Relationship Between Concentration of Urinary Biomarkers of Arsenic Metabolism and
• summarized in Table 1. Participants were, on average, 28 years old, had a BMI of 24 kg/m2, and approximately 40% were current smokers. The individuals
• included in this study do not meaningfully differ from the full cohort on any investigated covariates (Table 1). Participant characteristics by exposure status
• Table 3. Conventional Modeling: Linear Regression Results of Relative Proportion of Biomarkers of Arsenic Metabolism and Blood Pressure Metrics. All
• 1 InAs <9.12% (ref)
• 2 InAs <9.12% (ref)
• observed in the highest tertile of urinary arsenic exposure (for any of the As metabolites) and the trend was not significant (Table 2).
• blood pressure outcomes using linear regression models (Table 3). A higher percentage of urinary DMA was positively associated with systolic blood
• In the fully adjusted leave-one-out model (Table 4), a higher percentage of urinary DMA was positively associated with systolic blood pressure, pulse
• Table 4. Leave One Out Modeling: Linear Regression of the Relative Proportion of Two Biomarkers of Arsenic Metabolism (Third Left Out) and Blood Pressur
• 1 InAs MMA <12.39% (ref)
• MMA InAs <9.12% (ref)
• DMA InAs <9.12% (ref)
• 2 InAs MMA <12.39% (ref)
• MMA InAs <9.12% (ref)
• DMA InAs <9.12% (ref)
• Table 5. Raw Loadings of Principal Components in PCA Analysis.
• InAs% -0.875 -0.484
• principal components are presented in Table 5. Based on these loadings, the components were interpreted as follows: (1) principal component 1 (PC1)

Methods (brief)

• monomethylated arsenic (MMA), and dimethylated arsenic (DMA)) individually as a percentage of the sum of inorganic and methylated arsenic; (2) leave-
• vs. lower DMA% (>77.51% vs. ≤71.28% DMA over the sum of inorganic and methylated arsenic species) showed higher systolic blood pressure (β = 3.75
• models, higher DMA% (>77.51% vs. <71.28%) as a result of lower MMA%, was associated with higher systolic blood pressure (β = 7.24 mmHg; 95% CI: 2.25,
• findings. The second methylation step from MMA to DMA was associated with higher systolic blood pressure (β = 0.93 mmHg; 95% CI: 0.11, 1.75) and pulse
• Conclusions: Our findings suggest that biomarkers of efficient methylation of inorganic arsenic to DMA are associated with higher blood pressure compared
• acid (MMA3+), and then subsequently methylated to dimethylarsinic acid (DMA5+), which can be reduced to dimethylarsinous acid (DMA3+). The analysis
• percentage of each species over the sum of inorganic and methylated arsenic species: InAs%, MMA%, and DMA%) with systolic and diastolic blood pressure,
• ineligible if they reported hypertension medication use or if their blood pressure on enrollment was higher than 160/95 mmHg. Data were collected on each
• were missing blood pressure measures, and seven participants were missing data on body mass index (BMI) or water consumption. The final sample
• Spot urine samples were collected in the field before work on the third day of data collection and transferred to a nearby laboratory for aliquoting and on-site
• analyses. Urine osmolality was measured via a handheld refractometer and used as a covariate to adjust for urine dilution. Urine samples were then stored at
• The samples were thawed, and an aliquot (100 µL) was treated with hydrogen peroxide (30%wt, 10 µL) solution by volume. The resulting solutions were
• column for separation. InAs, MMA, and DMA were quantified using inductively-coupled plasma mass spectrometry with oxygen as a reaction gas. This
• details can be found in Glabonjat et al. (21). For quality control, the speciated arsenic samples were corrected by calibration background, instrumental drift,
• and method blanks. The method blanks were run alongside the urine samples and were prepared in the same manner to quantify any potential
• contamination in the sample. The standard deviation of the measured blanks was then multiplied by 3.33 to determine the method detection limit (MDL) (21).
• The MDL for InAs was 0.05 µg/L, that of MMA was 0.04 µg/L, and that of DMA was 0.03 µg/L. Any arsenic concentrations below the MDL were imputed with
• Total arsenic was calculated as the sum of InAs, MMA and DMA. The percentage of urinary arsenic species were calculated by the following equations:

Implications

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Wiki pages this source may touch

• Fish — marine, non-predatory (sardines, anchovies, salmon, cod)
• Arsenic

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