Non-Hodgkin’s lymphoma - Ethylene oxide exposure claim

Studies have shown that EtO exposure may cause the development of lymphoma

Several industries use ethylene oxide (EtO) in their processes. It’s mostly used as a pesticide and as a sterilizing agent. While it may be useful to businesses, EtO is actually categorized as a Group 1 human carcinogen by the IARC, EPA, and CDC.

A comprehensive paper published in 2023 has found that exposure to pesticides, including EtO, may increase the risks of developing non-Hodgkin’s lymphoma.

In another study, high exposure to EtO has been seen to elevate the likelihood of developing lymphoma by more than four times.

Workers and residents near EtO-emitting facilities have the highest chances of exposure, which may lead to the development of NHL. Listed below are the most common signs and symptoms of NHL:

• Swelling of lymph nodes, specifically in the neck, armpits, or groin
• Pain in the abdomen or bloating
• Chest pain or trouble breathing
• Fever and night sweats
• Weight loss

NHLs are generally classified as either B-cell or T-cell and are either indolent or aggressive. While there are over 70 kinds of NHL, the following are the most common NHL diagnoses:

• Angioimmunoblastic T-cell lymphoma (AITL)
• Burkitt lymphoma
• Cutaneous T-cell lymphoma
• Diffuse Large B-cell lymphoma (DLBCL)
• Follicular lymphoma
• Hepatosplenic gamma/delta T-cell lymphoma
• Lymphoblastic lymphoma
• Mantle cell lymphoma
• Marginal zone lymphoma
• Peripheral T-cell lymphoma (PTCL)
• Small lymphocytic lymphoma (SLL)
• Systemic anaplastic large cell lymphoma (ALCL)
• Waldenström macroglobulinemia (lymphoplasmacytic lymphoma)

Because of the many NHL types, it would be best to confirm with your respective physician whether or not your lymphoma diagnosis falls under the NHL group. If your doctor provides you with any type of NHL diagnosis that you suspect is due to EtO exposure, know that you may be entitled to legal compensation.

How ethylene oxide causes non-Hodgkin's lymphoma

Multiple authoritative health agencies classify ethylene oxide as a human carcinogen, and the evidence base includes epidemiological studies showing associations between EtO exposure and lymphoid cancers like non-Hodgkin's lymphoma:

• The U.S. Environmental Protection Agency explicitly lists non-Hodgkin lymphoma as one of the cancers for which human long-term EtO exposure increases risk
• The EPA explains that long-term inhalation exposure to EtO increases the risk of cancers of the white blood cells, including non-Hodgkin lymphoma, multiple myeloma, and lymphocytic leukemia
• The U.S. National Cancer Institute notes that epidemiological studies of occupational EtO exposures frequently report associations with lymphoma and leukemia

The biological mechanism linking EtO to NHL and other cancers is well established and recognized by regulatory bodies. Ethylene oxide operates as a direct-acting DNA alkylating agent, meaning it reacts chemically with DNA without needing metabolic activation. This creates DNA adducts and mutations in cells exposed to EtO.

When a person inhales ethylene oxide, the gas is absorbed through the lungs and distributed systemically throughout the body. This systemic distribution means that lymphoid tissues, including lymph nodes and circulating lymphocytes, become exposed to EtO and subject to its DNA-damaging effects. The chemical bonds that EtO forms with DNA bases interfere with normal cellular processes and create genetic instability.

EtO exposure produces dose-related increases in DNA and protein adducts and induces several types of genetic damage:

• DNA adducts that interfere with normal replication
• Chromosomal abnormalities that disrupt gene organization
• Mutations that alter the genetic code in lymphoid cells

Persistent DNA damage in vulnerable lymphoid precursor cells can trigger the transformation into cancer cells that defines lymphomas like NHL. Once lymphocytes collect enough mutations in their growth-control genes, they start multiplying without limits, creating the cancerous masses that characterize non-Hodgkin's lymphoma.

Case-control studies of workers have found higher lymphoma risk among those with moderate to high EtO exposure compared to unexposed controls. While the epidemiological evidence for NHL specifically gets classified as limited (studies demonstrate some positive associations without being uniformly conclusive alone), this evidence strengthens the overall carcinogenic classification alongside mechanistic findings.

The International Agency for Research on Cancer Monographs and the EPA's integrated risk assessments conclude that EtO is carcinogenic to humans and that epidemiological and mechanistic evidence support connections with lymphoid cancers, including NHL. Comprehensive toxicology profiles from CDC and ATSDR note that cohort studies suggest elevated risk of lymphohematopoietic cancers, which include non-Hodgkin lymphoma, in populations exposed to EtO.

EPA and IARC evaluations stress that EtO's ability to damage DNA is the primary basis for its carcinogenicity. This genotoxic mechanism affects lymphoid cells along with other cancer types associated with EtO. Although researchers continue studying the precise molecular pathways in human lymphoid tissues, the genotoxic activity of EtO offers a mechanistic explanation for its ability to trigger and advance cancers such as non-Hodgkin lymphoma.

The evidence supporting the connection between EtO and NHL includes:

• Epidemiological studies in humans reporting connections between EtO exposure and increased incidence of non-Hodgkin's lymphoma and other lymphoid cancers
• Biological mechanism showing EtO functions as a direct DNA alkylating agent, causing genotoxic damage capable of initiating and promoting malignant transformation in lymphoid cells
• Regulatory consensus from agencies like EPA and IARC considering EtO a human carcinogen, with evidence linking it to lymphoid cancers such as NHL

Long-term inhalation exposure to ethylene oxide is associated with increased risk of non-Hodgkin's lymphoma, supported by human epidemiological evidence and a well-characterized genotoxic mechanism that affects DNA in lymphoid cells.