Exposure to mercury from dental amalgam: actual contribution for risk assessment Original paper
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Metals
Metals
Heavy metals influence microbial pathogenicity in two ways: they can be toxic to microbes by disrupting cellular functions and inducing oxidative stress, and they can be exploited by pathogens to enhance survival, resist treatment, and evade immunity. Understanding metal–microbe interactions supports better antimicrobial and public health strategies.
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Divine Aleru
Read MoreI am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
Microbiome Signatures identifies and validates condition-specific microbiome shifts and interventions to accelerate clinical translation. Our multidisciplinary team supports clinicians, researchers, and innovators in turning microbiome science into actionable medicine.
I am a biochemist with a deep curiosity for the human microbiome and how it shapes human health, and I enjoy making microbiome science more accessible through research and writing. With 2 years experience in microbiome research, I have curated microbiome studies, analyzed microbial signatures, and now focus on interventions as a Microbiome Signatures and Interventions Research Coordinator.
What was studied?
This study measured how much mercury people absorb from dental amalgam work and from having amalgam fillings, using biological monitoring as the main readout. The authors collected first-morning urine and hair samples and quantified total mercury with atomic absorption spectrometry in winter 2017 and spring 2018, then tested whether mercury levels tracked with dental activity and with the number of fillings in the mouth. They framed the work as an updated contribution to risk assessment because dental amalgam remains a meaningful source of chronic mercury exposure in the general population and a potential occupational exposure for dental staff.
Who was studied?
The study included 50 volunteers: 40 dental personnel (dentists and staff) and 10 controls who did not perform amalgam-related work during the sampling period. Dental personnel averaged 64 amalgam procedures in the prior month (range 15–280) and reported a higher average number of their own amalgam fillings than controls, which allowed the authors to examine exposure from both work tasks and personal restorations. The participants spanned adult ages, with a mean age of 44 years in dental personnel and 56 years in controls, and the analysis treated urine mercury (normalized to creatinine) and hair mercury as the primary exposure markers.
What were the most important findings?
Measured mercury levels stayed well below the occupational biological limit for urine mercury, supporting the authors’ conclusion that current dental workplace exposure generally remains within acceptable risk bounds under modern practices. In dental personnel, the median urine mercury was 1.48 µg/g creatinine (maximum 17.14), while controls showed a median of 0.36 µg/g creatinine (maximum 2.74), and hair mercury medians were 0.340 µg/g in dental personnel versus 0.224 µg/g in controls. The authors found a modest relationship between the number of a person’s own amalgam fillings and urine mercury across all participants, while hair mercury did not track with filling count, and occupational workload metrics did not show a clear correlation with urine or hair mercury within dental personnel. Because this study did not measure the oral or gut microbiome, it does not define microbial signatures; however, it strengthens exposure phenotyping for future microbiome work by giving realistic biomarker ranges for dental-amalgam–related mercury exposure that researchers can pair with microbiome profiling.
What are the greatest implications of this study?
Clinically, these findings support a balanced message: modern dentistry practices appear to keep mercury exposure in dental staff below established biological limits, yet amalgam fillings still act as a continual, low-level source of mercury for people who have them. This matters for risk discussions because clinicians often face patient questions about chronic exposure, and this study reinforces that urine mercury can rise with the number of restorations even when levels remain low on an occupational scale. For microbiome-focused clinicians, the key implication is practical rather than mechanistic: urine mercury normalized to creatinine provides a feasible exposure marker to stratify patients in studies that test whether mercury exposure associates with oral or gut dysbiosis, barrier changes, or inflammatory profiles, without assuming those effects from exposure alone.
Mercury primarily affects microbiome pathogenesis by acting as a strong toxic selector that enriches organisms carrying mercury detox systems and the mobile elements that often co-carry antimicrobial resistance. In the gut, mercury speciation and bioavailability are shaped by thiols and sulfide chemistry, while microbial responses are dominated by the mer operon toolkit that detects Hg(II), traffics it intracellularly, and reduces it to Hg(0) for detox and loss from the cell.