Observational study finds pesticide exposure influences timing of puberty in Spanish girls — Evidence Review

Childhood exposure to certain pesticides may influence when girls experience their first menstrual period, with some chemicals linked to earlier onset and others to delays. Most related studies generally support a connection between pesticide exposure and altered puberty timing, though specific effects vary across compounds and populations, as seen in research published by the University of Granada.

• Research consistently finds that endocrine-disrupting chemicals (EDCs), including various pesticides, can shift the timing of puberty, but effects differ based on the type of compound and the developmental window of exposure 2 4.
• Several studies observe both earlier and later puberty linked to different pesticide exposures, mirroring the new study’s finding that ETU is associated with earlier menarche and TCPy with delays 2 4 5.
• The quality and consistency of evidence remain moderate; systematic reviews emphasize the need for more longitudinal research to clarify these associations and underlying mechanisms 1 2.

Study Overview and Key Findings

Concerns about the impact of environmental chemicals on child development have grown as evidence accumulates that some widely used pesticides can disrupt hormonal regulation. This study stands out by following a large, geographically diverse group of Spanish girls from childhood through adolescence, using biomarker-based exposure assessments to examine associations with the timing of menarche. The research is timely, given ongoing policy debates and regulatory efforts in the European Union and globally to limit pesticide use and exposure, especially among children.

Property	Value
Study Year	2026
Organization	University of Granada, ibs.granada Biomedical Research Institute
Journal Name	Environmental Research
Authors	Carmen Freire, Alicia Olivas-Martinez, Francesca Castiello, Alba Jimeno-Romero, Sara Lopez de Calle, Beatriz Suárez, Adonina Tardón, Marta M. Rodriguez-Suarez, Mònica Guxens, Martine Vrijheid, Andrea Beneito, Maria-Jose Lopez-Espinosa
Population	Girls aged 7 to 16 from Spain
Sample Size	n=506
Methods	Observational Study
Outcome	Timing of menarche related to pesticide exposure
Results	Higher ETU levels linked to earlier menarche, TCPy to later menarche.

Literature Review: Related Studies

To contextualize these findings, we searched the Consensus database (over 200 million research papers) using the following queries:

1. childhood pesticide exposure puberty timing
2. ETU menarche onset studies
3. TCPy effects on menstrual cycle

Below, we group related findings from these studies into key topics:

Topic	Key Findings
How do pesticides and EDCs influence puberty timing in children?	- Multiple studies report both advances and delays in puberty timing associated with pesticide exposure, with effects varying by compound and gender 2 4 5. - Non-persistent pesticides and other EDCs may affect puberty timing through hormone disruption mechanisms 2 4.
Are specific pesticides (e.g., organophosphates, PBDEs, dithiocarbamates) linked to earlier or later puberty?	- Organophosphates and some fungicide residues (like ETU) have been linked to both earlier and later puberty onset, depending on exposure window and body composition 2 5. - Persistent organic pollutants (POPs) such as PBDEs are associated with later puberty in girls 3 5.
What is the strength and consistency of evidence linking pesticide exposure to altered puberty?	- Systematic reviews highlight associations but note that evidence is generally of moderate-to-low quality, with inconsistent results and methodological limitations 1 2. - Longitudinal designs and biomarker-based exposure measures are recommended for future research 2 4.
Do body composition and gender modify the effects of pesticide exposure on pubertal development?	- Some studies suggest overweight or obese children may be more susceptible to delayed puberty linked to certain pesticide metabolites 2 4. - Sex-specific effects are observed: e.g., PBDE exposure may delay menarche in girls but accelerate pubic hair development in boys 4 5.

How do pesticides and EDCs influence puberty timing in children?

The new Spanish cohort study aligns with existing evidence that pesticide-related EDCs can shift puberty timing, but the direction and magnitude of these effects depend on the compound and context. Systematic reviews and cohort studies have found both earlier and later puberty associated with different chemicals, underscoring the complexity of endocrine disruption.

• Both advances and delays in puberty have been observed following exposure to non-persistent pesticides and other EDCs 2 4 5.
• Mechanisms likely involve interference with hormone signaling, including thyroid and sex steroids 2 4.
• Effects can vary by gender, with some EDCs accelerating puberty in boys while delaying it in girls 4 5.
• The new study’s finding of opposing effects for ETU (earlier menarche) and TCPy (later menarche) reflects these complex patterns 2 4 5.

Are specific pesticides (e.g., organophosphates, PBDEs, dithiocarbamates) linked to earlier or later puberty?

Evidence from related studies indicates that both the type of pesticide and the timing of exposure are critical to understanding effects on puberty. The new findings about ETU and TCPy add to documented associations between organophosphates, PBDEs, and altered puberty timing.

• PBDEs and organochlorine pesticides are linked to delayed menarche in girls 3 5.
• Organophosphate exposure, including chlorpyrifos (which metabolizes to TCPy), has been associated with both delayed and advanced puberty depending on context 2 5.
• Dithiocarbamate-type fungicide residues (such as ETU) may disrupt thyroid function, which is implicated in earlier puberty onset 2.
• The current study’s results are directly in line with these patterns, showing both earlier and later menarche depending on the chemical measured 2 3 5.

What is the strength and consistency of evidence linking pesticide exposure to altered puberty?

While most studies suggest a relationship between pesticide exposure and puberty timing, systematic reviews highlight limitations in study design, exposure assessment, and confounding control. As a result, findings are considered suggestive but not definitive.

• The evidence base is marked by moderate-to-low quality, with a need for standardized exposure and outcome measures 1 2.
• Consistency across studies is limited by differences in populations, exposure windows, and analytical approaches 2 4.
• Longitudinal biomarker-based studies, such as the new Spanish cohort, are recommended to strengthen causal inference 2 4.
• Reviews call for more research on specific pesticides and their mixtures, as well as interactions with nutrition and body composition 2 4.

Do body composition and gender modify the effects of pesticide exposure on pubertal development?

Emerging research indicates that the impact of pesticide exposure on puberty may be influenced by factors such as body mass index (BMI) and sex. The current study’s observation that TCPy-related delays in menarche were more pronounced in overweight or obese girls is consistent with this literature.

• Overweight and obese children may experience greater effects of endocrine disruptors on pubertal timing 2 4.
• Sex differences are notable: certain compounds delay puberty in girls but accelerate it in boys, and vice versa 4 5.
• Interactions between nutrition, body composition, and chemical exposure complicate interpretation of results 2 4.
• The present study’s subgroup findings reflect the importance of considering these modifying factors in research and policy 2 4 5.

Future Research Questions

Despite growing knowledge, significant gaps remain in understanding how childhood pesticide exposure affects puberty. Better longitudinal designs, more precise exposure assessments, and consideration of individual and environmental modifiers are needed to clarify causal pathways and health implications.

Research Question	Relevance
How do different pesticide classes (organophosphates, fungicides, herbicides) uniquely affect puberty timing in girls and boys?	Understanding class-specific effects is crucial for regulatory action and risk assessment, as different compounds may have opposite or additive effects on development 2 4 5.
What biological mechanisms underlie the opposing effects of ETU and TCPy on menarche timing?	Clarifying mechanisms will help explain why some EDCs accelerate and others delay puberty, guiding targeted interventions and risk communication 2 4.
Does body composition (BMI) modify the impact of pesticide exposure on pubertal development?	The interaction between BMI and chemical exposure may explain variability in effects and help identify vulnerable subpopulations 2 4 5.
Are early or delayed menarche due to pesticide exposure linked to long-term health risks (such as cancer or reproductive disorders)?	Long-term follow-up is needed to determine whether altered puberty timing from pesticide exposure translates into increased risk for later health problems 2 5.
What are the cumulative and interactive effects of multiple pesticide exposures on puberty?	Real-world exposures often involve mixtures, and understanding combined effects is critical for accurate risk assessment and public health guidance 2 4.