SummaryLow-dose exposures to common environmental chemicals that are deemed safe individually may be combining to instigate carcinogenesis, thereby contributing to the incidence of cancer. This risk may be overlooked by current regulatory practices and needs to be vigorously investigated.

Potentially carcinogenic compounds may cause cancer through direct DNA damage or through indirect cellular or physiological effects. To study possible carcinogens, the fields of endocrinology, genetics, epigenetics, medicine, environmental health, toxicology, pharmacology and oncology must be considered. Disruptive chemicals may also contribute to multiple stages of tumor development through effects on the tumor microenvironment. In turn, the tumor microenvironment consists of a complex interaction among blood vessels that feed the tumor, the extracellular matrix that provides structural and biochemical support, signaling molecules that send messages and soluble factors such as cytokines. The tumor microenvironment also consists of many host cellular effectors including multipotent stromal cells/mesenchymal stem cells, fibroblasts, endothelial cell precursors, antigen-presenting cells, lymphocytes and innate immune cells. Carcinogens can influence the tumor microenvironment through effects on epithelial cells, the most common origin of cancer, as well as on stromal cells, extracellular matrix components and immune cells. Here, we review how environmental exposures can perturb the tumor microenvironment. We suggest a role for disrupting chemicals such as nickel chloride, Bisphenol A, butyltins, methylmercury and paraquat as well as more traditional carcinogens, such as radiation, and pharmaceuticals, such as diabetes medications, in the disruption of the tumor microenvironment. Further studies interrogating the role of chemicals and their mixtures in dose-dependent effects on the tumor microenvironment could have important general mechanistic implications for the etiology and prevention of tumorigenesis.

Sequestration of plastics in sediments is considered the ultimate sink of marine plastic pollution that would justify unexpectedly low loads found in surface waters. Here, we demonstrate that mangroves, generally supporting high sediment accretion rates, efficiently sequester plastics in their sediments. To this end, we extracted microplastics from dated sediment cores of the Red Sea and Arabian Gulf mangrove (Avicennia marina) forests along the Saudi Arabian coast. We found that microplastics <0.5 mm dominated in mangrove sediments, helping explain their scarcity, in surface waters. We estimate that 50 ± 30 and 110 ± 80 metric tons of plastic may have been buried since the 1930s in mangrove sediments across the Red Sea and the Arabian Gulf, respectively. We observed an exponential increase in the plastic burial rate (8.5 ± 1.2% year−1) since the 1950s in line with the global plastic production increase, confirming mangrove sediments as long-term sinks for plastics.

Lysosomal responses in the digestive cells of Mytilus eduljs from 9 sites in Puget Sound, Washington. USA, with varying degrees of sediment contamination were measured using automatic image analysis. Mussels from urban-associated sltes (areas with elevated sediment concentration of anthropogenic contaminants such as PAHs, PCBs. DDTs, and toxic elements) showed pathological changes in the lysosomes (reduced lysosomal labilization period, reduced lysosomal stability and increased N-acetyl P-hexosaminidase activity), enhanced lipofuscin deposition and increased accumulat~on of lysosomal and cytoplasmic unsaturated neutral lipids. Morphometric measures of growth showed that mussels were generally smaller in size and that somatic tissue weight relative to shell length was lower in mussels from urban-associated sites relative to those from minimally contaminated sites. Highly significant correlations were observed between concentrations of tissue PAH, PCB, and selected toxic elements (measures of anthropogenic exposure) and lysosomal labil~zation period. Pathological alterations in the lysosomal system of mussels from the urban-associated sites were probably induced by the high tissue concentrations of organic and inorganic contaminants rather than as a result of potential confounding biotic (spawning stress) or abiotic (temperature, salinity and food availability) factors. The results show that cytochemical measurement of lysosomal responses combined with automatic image analysis have the potential to be used as sensitive, accurate and rapid techniques for assessing the biological impact of environmental contaminants in mussels in the near coastal environment.

Anthropogenic sea level rise (SLR) presents one of the greatest risks to human lives and infrastructures. Coastal vegetated ecosystems, that is, tidal marshes, seagrass meadows, and mangrove forests, elevate the seabed through soil accretion, providing a natural coastline protection against SLR. The soil accretion of these ecosystems has never been assessed in hot desert climate regions, where water runoff is negligible. However, tropical marine ecosystems are areas of intense calcification that may constitute an important source of sediment supporting seabed elevation, compensating for the lack of terrestrial inputs. We estimated the long‐term (14C‐centennial) and short‐term (210Pb‐20th century) soil accretion rates (SARs) and inorganic carbon (Cinorg) burial in coastal vegetated ecosystems of the Saudi coasts of the central Red Sea and the Arabian Gulf. Short‐term SARs (±SE) in mangroves of the Red Sea (0.27 ± 0.22 cm/year) were twofold the SLR for that region since 1925 (0.13 cm/year). In the Arabian Gulf, only mangrove forest SAR is equivalent to local SLR estimates for the period 1979–2007 (0.21 ± 0.09 compared to 0.22 ± 0.05 cm/year, respectively). Long‐term SARs are comparable or higher than the global estimates of SLR for the late Holocene (0.01 cm/year). In all habitats of the Red Sea and Arabian Gulf, SARs are supported by high carbonate accretion rates, comprising 40% to 60% of the soil volume. Further studies on the role of carbonates in coastal vegetated ecosystems are required to understand their role in adaptation to SLR.