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Updated: Mar 15, 2026
Measuring the Effect of Chemicals on the Growth and Reproduction of Caenorhabditis elegans
Published on: October 5, 2017
Editor's Highlight: Comparative Toxicity of Organophosphate Flame Retardants and Polybrominated Diphenyl Ethers to
Mamta Behl1, Julie R Rice1, Marjo V Smith2
1Division of the National Toxicology Program, National Institute of Environmental Health Sciences, NIH, Research Triangle Park, North Carolina.
Abstract:
With the phasing-out of the polybrominated diphenyl ether (PBDE) flame retardants due to concerns regarding their potential developmental toxicity, the use of replacement compounds such as organophosphate flame retardants (OPFRs) has increased. Limited toxicity data are currently available to estimate the potential adverse health effects of the OPFRs. The toxicological effects of 4 brominated flame retardants, including 3 PBDEs and 3,3',5,5'-tetrabromobisphenol A, were compared with 6 aromatic OPFRs and 2 aliphatic OPFRs. The effects of these chemicals were determined using 3 biological endpoints in the nematode Caenorhabditis elegans (feeding, larval development, and reproduction). Because C. elegans development was previously reported to be sensitive to mitochondrial function, results were compared with those from an in vitro mitochondrial membrane permeabilization (MMP) assay. Overall 11 of the 12 flame retardants were active in 1 or more C. elegans biological endpoints, with only tris(2-chloroethyl) phosphate inactive across all endpoints including the in vitro MMP assay. For 2 of the C. elegans endpoints, at least 1 OPFR had similar toxicity to the PBDEs: triphenyl phosphate (TPHP) inhibited larval development at levels comparable to the 3 PBDEs; whereas TPHP and isopropylated phenol phosphate (IPP) affected C. elegans reproduction at levels similar to the PBDE commercial mixture, DE-71. The PBDEs reduced C. elegans feeding at lower concentrations than any OPFR. In addition, 9 of the 11 chemicals that inhibited C. elegans larval development also caused significant mitochondrial toxicity. These results suggest that some of the replacement aromatic OPFRs may have levels of toxicity comparable to PBDEs.
Insights
Replacement organophosphate flame retardants (OPFRs) show toxicity comparable to phased-out polybrominated diphenyl ethers (PBDEs). Studies in Caenorhabditis elegans indicate similar effects on development and reproduction, highlighting potential health concerns with these new flame retardants.
Area of Science:
- Environmental toxicology
- Developmental toxicology
- Nematode toxicology
Background:
- Polybrominated diphenyl ethers (PBDEs) are being phased out due to developmental toxicity concerns.
- Organophosphate flame retardants (OPFRs) are increasingly used as replacements, but their toxicity is not well-characterized.
- Assessing the toxicological profiles of OPFRs is crucial for evaluating potential health risks.
Purpose of the Study:
- To compare the toxicological effects of PBDEs and OPFRs using Caenorhabditis elegans.
- To investigate the impact of these flame retardants on nematode feeding, larval development, and reproduction.
- To correlate observed biological effects with in vitro mitochondrial toxicity.
Main Methods:
- Toxicological screening of 4 PBDEs and 8 OPFRs (6 aromatic, 2 aliphatic) in C. elegans.
- Assessment of three biological endpoints: feeding rate, larval development, and reproductive output.
- Comparison of C. elegans results with an in vitro mitochondrial membrane permeabilization (MMP) assay.
Main Results:
- 11 of 12 flame retardants tested showed activity in at least one C. elegans endpoint.
- Triphenyl phosphate (TPHP) and isopropylated phenol phosphate (IPP) exhibited toxicity comparable to PBDEs in larval development and reproduction.
- PBDEs reduced feeding at lower concentrations than OPFRs, and most compounds inhibiting development also caused mitochondrial toxicity.
Conclusions:
- Some aromatic OPFRs demonstrate toxicity levels similar to PBDEs, suggesting potential risks associated with these replacements.
- Mitochondrial dysfunction may be a common mechanism of toxicity for these flame retardants.
- Further research is needed to fully understand the health implications of OPFR exposure.
