The study, conducted by Orhan Balıkçı and colleagues, collected data from 756 accounting and finance professionals in the Marmara region of Türkiye. This professional environment was chosen because these positions frequently require concentration, analytical abilities, and prolonged focus on individual tasks, making them ideal for assessing whether certain types of social distance might operate differently than traditional beliefs suggest.

Workplace loneliness is defined as the distressing feeling that arises when employees perceive a gap between the social relationships they desire at work and those they experience. Traditional loneliness research differentiates between emotional loneliness, which reflects the absence of close, meaningful, and emotionally supportive relationships, and social loneliness, which refers to a lack of broader social integration, group belonging, or network embeddedness. Although these dimensions are theoretically distinct, organizational studies have rarely explored whether they lead to different outcomes in workplace settings.

The theoretical framework draws on Need to Belong Theory, which proposes that individuals have a fundamental need to establish meaningful, stable, and satisfying interpersonal relationships. From this perspective, emotional loneliness reflects a more fundamental deficit in the quality of relational bonds, whereas social loneliness primarily concerns the extent of integration into broader social networks. The study also employs Conservation of Resources theory, suggesting that individuals strive to obtain and preserve valuable resources such as emotional energy, interpersonal support, and social belonging. In situations where these resources are lacking, stress, burnout, and a decline in performance may occur.

Two particularly pertinent mechanisms are wellbeing and job crafting. Wellbeing encompasses employees’ positive psychological functioning, vitality, and overall mental health, all of which are closely linked to sustained performance. Job crafting refers to employees’ proactive efforts to redesign tasks, relationships, or perceptions of work to enhance their fit and motivation. Employees experiencing loneliness may experience declines in wellbeing and become less inclined to engage in adaptive job crafting behaviors, which may subsequently affect performance.

The data were analyzed using a multistep analytical approach. Descriptive statistics and reliability analyses were conducted using SPSS 21, followed by confirmatory factor analysis to examine the construct validity of the measurement model. Mediation analyses were conducted using the PROCESS macro for IBM SPSS Statistics, with bootstrapping procedures using 5,000 resamples to obtain robust estimates of indirect effects. A mediation effect was considered significant when the 95% bootstrap confidence interval for the indirect effect did not include zero.

The findings indicate that emotional loneliness had a significant negative effect on employee performance (β = −0.3569, t = −12.5998, p < 0.001). When wellbeing was included as a mediator, the explanatory power of the model increased from 17.39% to 27.46%. Wellbeing had a significant positive effect on employee performance (β = 0.5277, t = 15.6317, p < 0.001), while the direct effect of emotional loneliness became statistically insignificant, indicating full mediation. Similarly, when job crafting was included as a mediator, the model’s explanatory power increased to 29.12%, with job crafting having a significant positive effect on performance (β = 0.6047, t = 16.3605, p < 0.001) and the direct effect of emotional loneliness becoming insignificant, again indicating full mediation.

In contrast, social loneliness had a significant positive effect on employee performance (β = 0.0817, t = 3.6131, p < 0.001). When wellbeing was included as a mediator, the model’s explanatory power increased substantially to 35.29%. Both social loneliness (β = 0.1752, t = 9.5746, p < 0.001) and wellbeing (β = 0.4811, t = 16.4592, p < 0.001) had significant positive effects on performance, with the direct effect of social loneliness remaining significant, indicating partial mediation. The bootstrapping results confirmed that the indirect effect of social loneliness on performance through wellbeing was statistically significant (Effect = 0.0393, 95% CI [0.0110, 0.0730]). Similarly, when job crafting was included as a mediator, the model’s explanatory power increased to 36.69%, with both social loneliness (β = 0.1720, t = 9.4959, p < 0.001) and job crafting (β = 0.5670, t = 17.1305, p < 0.001) having significant positive effects, again indicating partial mediation.

The positive relationship between social loneliness and employee performance may appear counterintuitive, but it suggests that limited social embeddedness does not necessarily produce negative outcomes in all settings. In occupations such as accounting and finance, where sustained attention, analytical thinking, and individual task focus are important, lower levels of social interaction may reduce distractions and allow greater concentration on core responsibilities. However, these findings should be interpreted cautiously, as they do not imply that social loneliness is inherently beneficial, but rather that its consequences may depend on job design, task characteristics, and organizational context.

The study makes several significant theoretical contributions. It demonstrates the inadequacy of considering workplace loneliness as a unidimensional experience that produces similar outcomes in all circumstances. The distinction between emotional and social loneliness is both theoretically meaningful and empirically significant in the organizational context. The findings also strengthen the explanatory power of belongingness theory by emphasizing that loneliness is more closely connected to the quality of relationships than to their quantity. From a practical standpoint, managers should not regard workplace loneliness as a uniform problem affecting all employees in the same way. Organizations should focus not only on ensuring that employees are physically present within a team but also on enabling them to build meaningful relationships, feel supported, and develop a sense of belonging. Employee engagement programs should not be limited to social events or superficial team activities; mentoring programs, climates of psychological safety, inclusive leadership behaviors, and meaningful feedback mechanisms can be more effective tools for alleviating emotional loneliness. Additionally, instead of standard practices that force all employees into constant social interaction, managers should develop more flexible management approaches that consider task structure and individual work preferences. Creating organizational environments that support job crafting behavior—allowing employees to redesign their tasks, adapt their work methods, and exercise greater autonomy—can reduce the negative effects of loneliness and strengthen employee performance.

Subject of Research: Organizational Psychology

Article Title: Not all workplace loneliness is harmful: the mediating roles of wellbeing and job crafting in the relationship with employee performance

Article References: Balıkçı, O., Elçi, M., Kitapci, H., Artar, M., & Sener, I. (2026). Not all workplace loneliness is harmful: the mediating roles of wellbeing and job crafting in the relationship with employee performance. Frontiers in Organizational Psychology, 4, Article 1876048. https://doi.org/10.3389/forgp.2026.1876048

Image Credits: AI Generated

DOI: 10.3389/forgp.2026.1876048

Keywords: workplace loneliness, emotional loneliness, social loneliness, employee performance, wellbeing, job crafting, organizational psychology, workplace, loneliness, harmful, mediating, roles

The research team, led by scientists investigating the mode of action (MoA) of lead chloride, employed three distinct model systems: the unicellular green alga Chlamydomonas reinhardtii strain 137C (wild type), the yeast Saccharomyces cerevisiae strain D7ts1, and the garden pea Pisum sativum L. cultivar Ran1. Each model was chosen for specific advantages. Chlamydomonas reinhardtii serves as a robust proxy for plant cells in genetic, molecular, physiological, and ecotoxicological studies, with results extrapolatable to a wide variety of plant organisms. Saccharomyces cerevisiae, whose fully sequenced genome shares around 31 percent similarity with the human genome, offers highly conserved stress-response pathways and protein similarity with higher eukaryotes including humans. Pisum sativum L., a classic plant model and one of the most important food items among legume crops, rounds out the trio.

The experimental design covered both short-term and long-term treatments. Cell suspensions of Chlamydomonas and yeast at a density of 1×10^6 cells per millilitre were treated with PbCl2 concentrations ranging from 0.45 to 3.6 mM for two hours. When the extremely low survival of the alga became apparent at this range, researchers added lower concentrations of 0.03, 0.06, 0.11, and 0.22 mM. Pea seeds were treated for 24 and 48 hours to evaluate germination and root length, while pea plants were grown for up to 10 days in contaminated medium at concentrations of 0.45 to 2.7 mM. The highest concentration of 3.6 mM was excluded from long-term experiments because it caused outright plant death.

The results exposed dramatic genotype-related differences in the response to lead treatment. When treated with concentrations in the range of 0.45–3.6 mM, Saccharomyces cerevisiae showed a dose-dependent decrease in cell survival down to 25 percent, while Chlamydomonas reinhardtii dropped to around 10 percent survival across all concentrations tested. Based on survival data, the team calculated that an approximately 30-fold lower dose can cause 50 percent lethality in the alga compared with the yeast. In other words, concentrations that barely trouble the yeast are devastating for the alga, a finding with important implications for how we choose sentinel organisms in environmental monitoring.

Perhaps the most striking discovery concerns DNA damage. Using constant field gel electrophoresis (CFGE), the researchers measured the induction of DNA double-strand breaks (DSBs), the most dangerous form of DNA lesion. For the first time, experimental evidence was obtained that PbCl2 induces DSBs in both Chlamydomonas reinhardtii and Saccharomyces cerevisiae. A statistically significant dose-dependent increase in DSBs was found in the alga at concentrations up to 0.11 mM, corresponding to the LD80. Treatment with 0.45 mM resulted in significant DNA degradation. Interestingly, when concentrations corresponding to equivalent lethality doses were compared across the two organisms, both showed around a 2-fold induction of DSBs at LD80, suggesting a shared underlying mechanism despite the vastly different concentration ranges required.

Crucially, no mutagenic effect was detected in either unicellular model. The mutagenic index in Chlamydomonas was calculated to be less than 2.5, indicating no mutagenic capacity, while mitotic gene conversion and reverse mutations in yeast were comparable with untreated controls. This provides indirect evidence that PbCl2 toxicity at the tested concentrations is not related to point mutations, impaired cell division, micro-chromosomal aberrations, mitotic gene conversion, or mitotic crossing-over. The damage appears to be clastogenic rather than mutagenic, breaking DNA strands rather than altering their sequence.

The pro-oxidative potential of PbCl2 was confirmed in all model systems, covering a wide range of reactive oxygen species (ROS). In yeast, a dose-dependent increase in superoxide anion levels was measured, with more than 2-fold higher levels at LD80, alongside elevated malondialdehyde (MDA) and depleted glutathione (GSH). The reduction in GSH likely reflects the high affinity of the GSH thiol group to lead, forming Pb-GSH complexes in the cytosol. In Chlamydomonas, a dose-dependent increase in intracellular peroxides (H2O2) was obtained, with more than 3-fold higher levels of both MDA and H2O2 at concentrations causing over 80 percent cell lethality. In pea plants, the most pronounced oxidative stress was observed after 10 days of growth in medium contaminated with 2.7 mM PbCl2, with MDA levels rising to 166 percent and H2O2 to 172 percent of controls.

Correlation analysis strengthened the mechanistic picture. In Chlamydomonas, the decrease in cell survival corresponded strongly with increases in H2O2 and DSBs, and higher H2O2 levels correlated with low levels of all photosynthetic pigments. In yeast, the decrease in cell survival correlated strongly with superoxide anion induction, while DSB increases correlated with MDA elevation and GSH depletion. Based on these relationships, the researchers speculate that Pb-induced oxidative stress, particularly in terms of intracellular peroxides, probably participates in the induction of DSBs, which in turn may partially result in cell death. The study provides new evidence that PbCl2 can affect both the DNA molecule and photosynthetic pigments via the induction of oxidative stress.

The photosynthetic machinery took a significant hit in both plant models. All photosynthetic pigments in Chlamydomonas and Pisum sativum decreased by around 40–60 percent in both experimental schemes, without concentration or time dependence. In the alga, chlorophyll a, chlorophyll b, and carotenoids dropped by around 50–60 percent. Some authors attribute lead’s effect on chlorophyll to its ability to replace magnesium in the chlorophyll ring, while others propose that Pb-induced disturbance of photosynthesis in microalgae is a major cause of cell death. In this study, however, no statistically significant correlation was obtained between pigment levels and cell survival, pointing instead to H2O2-mediated growth inhibition as the more likely pathway.

The toxicity of PbCl2 on pea plants proved surprisingly mild. Around 10 percent inhibition of seed germination and around 20 percent root length reduction were measured at concentrations equal to or higher than 1.8 mM. While statistically significant, these effects can hardly be regarded as significant from a biological point of view, confirming previous observations that growth-related parameters are not the most sensitive endpoints for evaluating lead toxicity. The stronger effect on root length than germination may be due to the low permeability of the seed testa to lead.

The finding that Chlamydomonas reinhardtii is a sensitive test system towards PbCl2 contributes to good strategies for revealing very low levels of contaminants present chronically in main environmental matrices. Very sensitive genotypes are excellent tools for detecting chronic low-level contamination that can result in long-term disturbance of biota. The study’s proposed approach, a battery of test systems with various endpoints, could be considered a promising tool in the ecotoxicological assessment of various xenobiotics, in line with WHO recommendations that multiple test systems and endpoints evaluating different adverse effects at different levels provide the most reliable information about the mode of action of environmental contaminants.

Subject of Research: Genotype differences towards lead chloride harmful action

Article Title: Genotype differences towards lead chloride harmful action

Article References: Todorova, T. I., Parvanova, P. N., Boyadzhiev, K. P., Dimitrov, M. D., & Chankova, S. G. (2023). Genotype differences towards lead chloride harmful action. BioRisk, 20, 37-57. https://doi.org/10.3897/biorisk.20.97598

Image Credits: AI Generated

DOI: 10.3897/biorisk.20.97598

Keywords: Genotype, differences, towards, lead, chloride, harmful, action, scientific research

FSHD is among the most common hereditary neuromuscular disorders, affecting roughly 5 in 100,000 people worldwide. Unlike Duchenne muscular dystrophy, it does not shorten life expectancy, but its progressive nature exacts a heavy toll. The disease stems from a genetic error on chromosome 4: a contraction of D4Z4 macrosatellite repeats causes hypomethylation of the region, allowing sporadic expression of DUX4, a transcription factor normally silent in mature skeletal muscle. DUX4 switches on germline and early stem cell genes that should never be active in adult muscle, disrupting cellular homeostasis and triggering inflammation and apoptosis. The result is a progressive, asymmetric loss of muscle mass that typically begins in the face, shoulder girdle, and upper arms, later spreading to the trunk and lower limbs. Severity varies enormously: up to 30 percent of genetic carriers report no symptoms, while approximately 20 percent become wheelchair-dependent.

The pathological picture is more complex than simple muscle wasting. Quantitative MRI reveals fatty infiltration two to three times greater than in age-matched controls, along with STIR hyperintensity lesions—pockets of edema interpreted as signs of active inflammation. Muscle biopsies from STIR-positive regions show mononuclear cell infiltrates, elevated expression of major histocompatibility complex I, and greater collagen deposition, indicating fibrosis. Oxidative stress compounds the damage: transcriptomic analyses show upregulation of TNFα pathway genes, FSHD myoblasts display increased susceptibility to oxidative injury, and patients carry a reduced ratio of reduced to oxidized glutathione in their blood. Critically, these radiological features—fatty infiltration, lesion burden, and shrinking muscle volume—are the most sensitive markers of progression, detectable within a single year, while functional scores often lag behind.

Weakness in FSHD exceeds what muscle loss alone can explain. Individuals consistently show reductions in maximal voluntary contraction force of more than 40 percent compared with controls, and even after correcting for fatty infiltration, specific force—the force per unit of contractile cross-sectional area—remains reduced by over 30 percent. Yet isolated single muscle fibers from the same patients generate nearly normal specific force. This paradox points the finger away from the contractile machinery itself and toward collective impairments: MRI-based estimates of contractile area likely overstate true fiber area because they cannot distinguish fibrosis, edema, and interstitial cells from contractile tissue. Emerging evidence also implicates defective excitation–contraction coupling. Meta-analyses reveal downregulation of genes associated with neuromuscular junction architecture, single-fiber electromyography shows abnormal transmission correlated with disease duration, sarcolemmal reorganization increases the distance between the sarcolemma and the nearest myofibril—potentially disrupting the T-tubule network—and muscle excitability studies reveal partial depolarization of the resting membrane potential, which could inactivate voltage-gated sodium channels and attenuate calcium release from the sarcoplasmic reticulum.

Against this backdrop, the review defines high-load resistance training precisely: programs using loads of 70 to 90 percent of one-repetition maximum, or the 4 to 12 repetition maximum range, which meta-analyses show are most effective at simultaneously increasing muscle mass and maximal strength. The authors emphasize that while lighter loads produce comparable hypertrophy when volume is matched, higher loads yield greater strength gains. Optimal prescription involves at least four sets per muscle group per week—ideally ten or more for maximizing hypertrophy—rest intervals of one to two minutes between sets, a minimum frequency of two weekly bouts, and progressive overload, in which loads are increased over time to maintain the targeted repetition range at near-maximal effort.

The acute responses to such training are well characterized in healthy populations. A single bout causes rapid neuromuscular fatigue, myofibrillar disruption visible under electron microscopy, mild swelling lasting up to 48 hours, soreness persisting for days, and elevated serum creatine kinase. Plasma cytokines such as IL-6, IL-1ra, MCP-1, and G-CSF rise transiently, and severe disruption is followed by mononuclear cell infiltration—collectively termed exercise-induced muscle damage. Crucially, these responses are normal remodeling processes, not signs of intolerance. Healthy individuals recover within days and are protected against comparable damage in subsequent bouts, a phenomenon known as the repeated bout effect. Meanwhile, anabolic signaling through MAPK pathways and mTORC1 drives muscle protein synthesis that remains elevated beyond 48 hours, while protein degradation returns to baseline—the cumulative imbalance producing net accretion of contractile protein.

Long-term, the benefits are substantial. Twelve to 24 weeks of high-load resistance training typically increases one-repetition maximum by 20 to 50 percent, with early gains driven primarily by neural adaptations—increased motor unit recruitment and discharge rate within the first two to four weeks—before morphological hypertrophy of roughly 5 to 20 percent becomes detectable. Strength gains translate into improved gait speed, chair stand performance, and balance, the very capacities that underpin independence. Equally relevant to FSHD, evidence from other populations shows that resistance training reduces fatty infiltration in older and overweight adults, attenuates chronic low-grade inflammation as measured by C-reactive protein, reduces oxidative stress markers in metabolic conditions, and—strikingly—alters inflammatory gene expression and reduces interstitial fibrosis in myositis, an autoimmune myopathy that shares mononuclear infiltration, fatty infiltration, fibrosis, and muscle fiber regeneration with FSHD.

So where did the caution come from? The review traces much of the dogma to two influential studies. Over 50 years ago, Johnson and Braddom reported that most members of an FSHD family were weaker in their dominant arm—the one used habitually—and concluded that extensive use, including resistance training, accelerates disease progression. But the conclusions were never substantiated by statistical analysis, and the methods were described only vaguely. Brouwer and colleagues later found statistically significant side-to-side differences in just 3 of 10 strength tests, with small numerical differences relative to large standard deviations. Subsequent studies across 102 individuals with FSHD found no effect of handedness on weakness patterns, and a case report in monozygotic twins reached the same conclusion. The overwork weakness hypothesis, in other words, does not withstand replication.

The recommendation to avoid loads above 30 percent of one-repetition maximum fares no better. Several resistance training studies have included individuals with FSHD who repeatedly lifted loads well above that threshold, and all reported the training was well tolerated, with most showing moderate improvements in strength and function. On eccentric contractions, the review notes that submaximal eccentric actions—inevitable in daily activities like sitting down—are demonstrably safe, and the only study to test maximal eccentric contractions found that individuals with myopathic disease showed slightly attenuated signs of exercise-induced muscle damage compared with healthy controls, whose creatine kinase rose significantly more three days post-exercise. Though limited to two individuals with FSHD, the study gives no indication of heightened vulnerability. Persistent soreness, the authors add, is the expected response of any untrained person beginning training—not evidence of disease provocation—and clinicians should avoid language that reinforces a sense of fragility, which fuels fear and exercise avoidance.

The most cited study on the topic, published by van der Kooi and colleagues in 2004, trained 19 individuals with FSHD for 52 weeks and is frequently invoked as proof that resistance training offers no benefit. Yet the review highlights critical limitations: the program started with 10RM loads progressing toward 5RM—below the high-load definition—lacked a healthy positive control group, and produced a 37 percent increase in elbow flexion one-repetition maximum that has been overshadowed by emphasis on its negative findings. No available study has adequately addressed whether high-load training affects the major pathological features of FSHD, considered the disease’s inherent asymmetry, or employed gold-standard whole-body MRI to track fibrosis, fatty infiltration, and muscle mass. Until such trials are conducted, the authors conclude, patients and clinicians will remain without answers about an intervention that is accessible, inexpensive, and likely low-risk—one that could delay the mobility decline and loss of independence that define advanced FSHD.

Subject of Research: FSHD

Article Title: High-load resistance training and FSHD: harmful mixture or a silver bullet combination?

Article References: Meinhold, M., & Hornberger, T. A. (2026). High-load resistance training and FSHD: harmful mixture or a silver bullet combination?. Journal of Neurology, 273(10), Article 605. https://doi.org/10.1007/s00415-026-14148-7

Image Credits: AI Generated

DOI: 10.1007/s00415-026-14148-7

Keywords: FSHD, resistance training, muscular dystrophy, exercise science, neuromuscular disorders, DUX4, muscle physiology, High-load, resistance, training, harmful, mixture

The study, published in the journal Global Biogeochemical Cycles, was led by John Harrison, the Edward R. Meyer Distinguished Professor in WSU’s School of the Environment. Harrison, who directs the Global Change and Watershed Biogeochemistry Laboratory, noted that while the ocean is vast, the contribution of land-based nutrients to coastal zones has been a subject of debate among oceanographers. The research aims to resolve this uncertainty by integrating data on what enters coastal waters from land with data on offshore marine sources. The findings suggest that the scientific community studying the coastal impacts of land-based nutrients has been correct in emphasizing the importance of these inputs.

Human activities introduce nitrogen and phosphorus into rivers and coastal waters through various pathways. These include fertilizer and manure runoff from agricultural lands, wastewater emissions from sewage systems, urban runoff from lawns and streets, and emissions from vehicles and power plants. The researchers developed a novel database that covers global sources of nitrogen, phosphorus, and silicon across both pre-industrial and contemporary time spans. This database allows for an evaluation of how land-based human activities have altered nutrient ratios and increased the potential for eutrophication, a condition that promotes excessive algae growth and degrades water quality.

One of the key findings of the study is that while natural marine sources remain the largest overall contributor of nutrients globally, land-based sources constitute the majority of nutrients for more than half of the world’s coastlines. This indicates that in a substantial number of coastal regions, the balance of nutrient input is dominated by terrestrial processes rather than open-ocean dynamics. The study distinguishes between different types of nutrients, noting that the impact of human activity varies significantly depending on the specific element being measured.

Regarding nitrogen, the research found that human activities add more nitrogen than all natural sources in approximately a quarter of the planet’s coastal waterways. This human-driven excess is also evident in a fifth of the Large Marine Ecosystems, which are the large ocean areas extending outward from the coasts. For phosphorus, the human contribution exceeds natural sources in 11% of coastal waterways. These figures underscore the localized but significant nature of nutrient pollution, where specific regions experience disproportionate impacts due to concentrated human activity and land use practices.

The influence of human activity on silicon presents a contrasting trend. Rather than increasing levels, human activities tend to lower silicon levels in coastal waters. A primary mechanism for this reduction is the construction of river dams, which block the natural flow of silicon from land to the coast. Silicon is essential for certain marine organisms, such as diatoms, and its reduction can have cascading effects on marine food webs. This finding highlights that nutrient pollution is not a uniform issue; while some nutrients are being added in excess, others are being depleted, both of which can disrupt the delicate balance required for healthy marine ecosystems.

The study identifies specific geographic areas of greatest concern, including the Gulf of Mexico and the coastlines surrounding Europe and Asia. These regions are characterized by high levels of human impact and significant nutrient loading. By pinpointing these areas, the research provides a framework for prioritizing management efforts. Harrison emphasized that understanding where nutrient inputs are most critical is essential for effective resource allocation. The study serves as a first step in creating a framework to manage coastal zones efficiently, ensuring that mitigation strategies are directed where they will have the most substantial impact.

Several strategies could be adopted to reduce the nutrient load entering rivers and coastal waters. These range from implementing advanced technology in wastewater treatment plants to improving fertilizer management practices and adopting no-till farming methods. The study identifies areas where the health of coastal waters could be directly improved by changes in human contributions. Harrison noted that there are stretches of coastline globally where a significant increase in nutrient inputs would push the ecosystem into a danger zone, while a significant decrease would remove it from that zone. This distinction is crucial for policymakers and managers, as it identifies locations where intervention can yield clear benefits versus areas where high natural background nutrient loads may complicate management efforts.

The research underscores the importance of a holistic approach to coastal management. By integrating data on land, sea, and human inputs, the study provides a more complete picture of nutrient dynamics than previous global assessments. The findings suggest that while the challenge is significant, targeted interventions can make a meaningful difference. As coastal populations grow and economic activities intensify, the need for precise data to guide management decisions becomes increasingly urgent. The study offers a valuable tool for scientists, policymakers, and stakeholders seeking to protect the health and productivity of the world’s coastal waters.

Subject of Research: Marine Science

Article Title: Study maps where humans are driving harmful nutrient levels along coasts

Article References: Study maps where humans are driving harmful nutrient levels along coasts. (n.d.). Original publication

Image Credits: AI Generated

DOI: Not provided

Keywords: coastal ecosystems, nutrient pollution, nitrogen, phosphorus, silicon, eutrophication, Washington State University, Global Biogeochemical Cycles, maps, humans, driving, harmful